Resistance to AKT inhibitors in breast cancer, for example, can be caused by TSC1/2 loss, which activates mTORC1 and blocks apoptosis in a BAK-dependent manner, even with a reduced level of phosphorylated AKT, possibly by mTORC1-mediated translational control of Mcl-1, and can be overcome by combining AKT inhibitors with an Mcl-1 inhibitor [332, 333]. The gene discussed is AKT1; the disease is breast carcinoma.