The better efficacy of mTOR inhibitor and AKT inhibitor than other targeted agents was evident, as up to 40% bladder cancer cases showed constitutive activation of the PI3K/AKT/mTOR pathway resulting from either the deletions or mutations of tumor suppressor genes such as PTEN and TSC1 or the amplification or mutations of proto-oncogenes such as PI3KCA and AKT1 [9]. This evidence concerns the gene AKT1 and urinary bladder cancer.