Interestingly, breast cancer cell lines resistant to the AKT inhibitors capivasertib and MK-2206 express high levels of SGK1 and are sensitive to SGK knockdown (KD) [264], while sustained AKT inhibition leads to increased SGK3 expression that can replace AKT-mediated activation of mTORC1 [257]. The gene discussed is AKT1; the disease is breast cancer.