Moreover, it inhibited the function of phosphorylated AKT (p-AKT), cyclin D1, and cyclin-dependent kinases 4 while promoting the expression of phosphorylated breast cancer susceptibility protein, p-ATM, p53, p21, p38, Bax, and Bid, eventually evoking S phase arrest and apoptosis in bladder cancer cells. This evidence concerns the gene AKT1 and urinary bladder carcinoma.