Previous studies have shown that histone acetylation plays an important role in regulating the tumor microenvironment (TME), and histone deacetylase (HDAC) inhibitor CM-1758 can increase CD8+ T cell infiltration and promote macrophage polarization toward M1-like in the TME of BLCA patients, representing an attractive target for immunotherapy29. This evidence concerns the gene HDAC9 and bladder transitional cell carcinoma.