The fact that neither siRNA-mediated Akt silencing nor co-treatment with the PI3K inhibitor BKM120 further increased the inhibitory effects of SIP-SII, while forced expression of a constitutively active Akt mutant reversed such effects, proves that SIP-SII effectively inactivates Akt at low micromolar doses in bladder cancer cells. The gene discussed is PIK3CA; the disease is urinary bladder cancer.