Comprehensive studies have defined the molecular subtypes in bladder carcinoma, mainly by analyzing gene expression data, specific mutations, and copy-number changes with recent analyses suggesting that specific genetic alterations in fibroblast growth factor receptor 3 (FGFR3), tumor protein P53 (TP53), retinoblastoma 1 (RB1), Erb-B2 receptor tyrosine kinase 2 (ERBB2), nuclear-factor, erythroid 2 like 2 (NFE2L2), and lysine demethylase 6A (KDM6A/UTX) are enriched in different molecular subtypes and are clinically actionable [6,7,8]. This evidence concerns the gene TP53 and urinary bladder carcinoma.