Based on the notion that ERK mediated phosphorylation of MYC Ser-62 results in stabilization of the MYC protein, and activated AKT phosphorylates and inactivates GSK3, thereby inhibiting the phosphorylation of MYC at Thr-58 that promotes MYC degradation, it is possible that both the ERK and AKT pathways may be involved in the regulation of MYC protein stability in bladder cancer with aberrant FGFR3 activation (Fig. 3) [116, 125, 126, 128]. The gene discussed is AKT1; the disease is urinary bladder cancer.