Interestingly, DPYSL2 was also classified as one of 12 genes significantly associated with the prognosis of bladder cancer patients, and its high expression is associated with a favorable prognosis in bladder cancer patients [42]. It has been revealed that DPYSL2 was significantly upregulated in urinary bladder cancer compared to normal tissue, and the higher the expression, the more advanced the cancer stage. Moreover, DPYSL2 deficiency inhibited the malignant behavior and epithelial–mesenchymal transition in bladder cancer cells [43], thus the downregulation of DPYSL2 observed in the UBT after RTX administration may suggest the anti-cancer properties of the toxin. In urology, RTX is mostly used for the treatment of functional neurologic dysfunctions. Cancer studies investigating RTX primarily explore its analgesic properties for managing severe pain in advanced stages [44]. However, a recent study by Farfariello et al. [45] has also explored the potential anti-cancer effects of RTX, particularly in bladder cancer. This study demonstrated that RTX induces cell death in bladder cancer cells through mitochondrial dysfunction, leading to increased reactive oxygen species production and altered ADP/ATP ratios. In vivo, RTX administration resulted in reduced tumor growth in a xenograft mouse model of bladder cancer. These findings suggest that RTX’s cytotoxic effects on bladder cancer cells are mediated by disrupting mitochondrial function. While these studies provide preliminary evidence supporting RTX’s anti-cancer potential in bladder cancer, further research is necessary to fully elucidate its therapeutic efficacy and safety in clinical settings. The present study has also identified genes other than DPYSL2, whose altered expression may reflect RTX anti-cancer properties. For instance, RTX administration has been followed by the downregulation of the chaperonin containing TCP1 subunit 4 (CCT4) gene. Interestingly, the current research revealed 34 correlations between DEGs and other RNA in RTX UBT, and DPYSL2 and CCT4 genes formed the most connections based on expression profiles with other RNA. CCT4 is a part of the chaperonin-containing t-complex significant in cell cycle-related protein degradation [46]. CCT4 overexpression has been revealed in cancer cells compared with normal tissue, and the lack of CCT4 was found to promote apoptosis of cancer cells [47]. Thus, the observed downregulation of the CCT4 is consistent with RTX’s potential anti-cancer role. Moreover, the current data revealed the downregulation of DNA topoisomerase II Alpha (TOP2A) in RTX-treated UBT. In urinary bladder cancer, TOP2A has been suggested to be one of the potential therapeutic targets and a prognostic biomarker, as its overexpression has been strongly linked to the progression of the tumor stage and poor prognosis [48]. Moreover, in bladder urothelial carcinoma, the knockdown of TOP2A significantly reduced cancer cell proliferation [49]. The overexpression of this gene has been reported in several cancer types, including bladder cancer, and its upregulation has related to an increased risk of metastasis due to intensified migration of cells and inhibited apoptosis [48]. Additionally, the current study revealed other DEGs previously linked with cancer, such as the downregulated genes LIM zinc finger domain containing 2 (LIMS2; also known as PINCH2) and jagged canonical Notch ligand 1 (JAG1). It has been found that LIMS2 is involved in cell migration and adhesion via integrins and its deletion or downregulation correlated with promoting invasion and metastasis in several cancer types [31,50]. On the other hand, JAG1 is a critical Notch ligand that initiates Notch signaling through cell–cell interactions. Its overexpression has been documented across multiple cancer subtypes and is correlated with a poor clinical prognosis. Additionally, JAG1/Notch signaling pathways activate multiple oncogenic factors that govern cellular processes including proliferation, metastasis, chemoresistance, and angiogenesis. Consequently, the reduced expression of JAG1 may potentially suppress JAG1/Notch signaling activity and exhibit an anti-cancer effect. In the RTX-treated UBT, the current study revealed the upregulation of presenilin 1 (PSEN1). Presenilins are essential functional components of γ-secretase, an enzyme responsible for cleaving several transmembrane proteins. Studies have implicated PSEN1 dysfunction in both Alzheimer’s disease and cancer [51,52,53]. Growing evidence suggests a role for presenilins in carcinogenesis; however, their precise function in cancer development remains unclear. For instance, it has been found that PSEN1 overexpression reverses multi-chemoresistance in breast cancer by DNA initiating the damage response pathway [54]; conversely, PSEN1 expression was notably elevated in patients diagnosed with gastric cancer [53].