We recently showed that development of lapatinib resistance can be mediated through a switch in the regulation of cell survival from ErbB2-ErbB3-PI3K signaling in treatment naïve ErbB2+ breast cancer cells to ErbB3-EGFR-PI3K-PDK1-Akt (T308) signaling axis in the resistant setting, the latter driven in part through autocrine production of the ErbB3 ligand heregulin β1[16]. This evidence concerns the gene EGFR and breast carcinoma.