Recent studies in breast cancer cells demonstrated that treatment with a dual mTORC1/2 inhibitor AZD8055 led to increased expression and activation of several RTKs including the ERBB receptor family (ERBB1-4), IGF1R, and insulin receptor (IR), resulting in phosphoinositide-dependent kinase-1 (PDK1)–dependent activation/phosphorylation of Akt T308 (31). The gene discussed is IGF1R; the disease is breast cancer.