FGFR3 and in situ carcinoma: The onset of NMIBCs may be derived via simple hyperplasia and minimal dysplasia through the loss of heterozygosity of chromosome 9 and activating mutations of FGFR3, PIK3CA and STAG2. Invasive carcinomas could be due to TP53 mutation in addition to chromosome 9 deletions, but generally without FGFR3 mutations via flat dysplasia and carcinoma in situ [4].