Many key pathways and genetic alterations contribute to its pathogenesis: FGFR3 mutations promote tumor proliferation in NMIBC [4], TP53 and RB1 loss drive genomic instability in MIBC [5]; KDM6A mutations disrupt chromatin remodeling, aiding tumor progression [6]; PI3K-AKT-mTOR activation supports survival and growth [7]; PD-L1 overexpression through PD1 enables immune evasion [8]; Nectin-4 and Trop-2 overexpression enhance tumor adhesion, invasion, and progression, serving as targets for Enfortumab Vedotin and Sacituzumab Govitecan, respectively [9, 10] (Figure 1). The gene discussed is TACSTD2; the disease is neoplasm.