This variability reflects the existence of two distinct carcinogenic pathways: one driven by hyperplasia, which gives rise to low-grade (LG) NMIBC and is marked by the activation of oncogenes such as FGFR3 and RAS; and another associated with dysplasia and/or carcinoma in situ (CIS), leading to MIBC through alterations in tumor suppressor genes like TP53, RB1, and PTEN. Here, FGFR3 is linked to in situ carcinoma.