In a study involving cell lines harboring FGFR1, FGFR2 and FGFR3 alterations, which included bladder cancer cell lines (UMUC14 & RT112), ectopic expression of undegradable mutant MYC conferred resistance to FGFR inhibition while FGFR inhibitor treatment reduced ectopically expressed wild type MYC, suggesting the important role of FGFR activation in maintaining MYC stability and blockage of FGFR signaling causes downregulation of MYC mainly due to protein degradation [136]. This evidence concerns the gene MYC and urinary bladder cancer.