We found that mTORC1 activation in ErbB2+ breast cancer cells was exquisitely sensitive to c-Src activity through a tumor cell-intrinsic mechanism involving bioenergetic reprogramming, rather than modulation of growth factor-dependent pathways such as PI-3K/Akt33,34 or changes in the expression of mTORC1 subunits. The gene discussed is SRC; the disease is breast carcinoma.