Although the GSH conjugation function of GSTs can neutralize electrophilic endogenous and xenobiotic compounds by introducing a GSH molecule into them [30], GSTM5 overexpression accompanied by GSH decreasing did not affect the cytotoxic sensitivity of cisplatin and mitomycin C. This suggests that GSTM5 induction may be a potential strategy for bladder cancer treatment without inducing significant resistance to cisplatin and mitomycin C. GSTM5 overexpression slightly increased resistance to doxorubicin in 5637 cells (Figure 8A), increasing the IC50 from 3.2 μM (5637VC) to 5.2 μM (5637ovGSTM5). Here, GSTM5 is linked to urinary bladder cancer.