This conclusion is supported by a recent study demonstrating that activation of AKT signaling is a mechanism of acquired resistance to BGJ398 in lung and bladder cancer cell lines carrying activating FGFR alterations, and that such resistance can be efficaciously overcome by treatment with the AKT inhibitor GSK2141795 or by AKT silencing [34]. The gene discussed is AKT1; the disease is urinary bladder carcinoma.