We investigated the mechanisms by which inhibiting endogenous H2S production attenuates bladder tumor progression and enhances the anti-cancer effects of GEM using immunohistochemical (IHC) staining for markers of apoptosis (caspase-9 and poly [ADP-ribose] polymerase 1 (PARP-1)), neovascularization (vascular endothelial growth factor (VEGF)), proliferation (antigen Ki-67 (Ki67)), and immune-cell infiltration including macrophages (F4/80 and CD163) and T cells (CD8 and CD4) (Figure 4A). The gene discussed is MKI67; the disease is urinary bladder neoplasm.