These findings made it tempting to speculate that escape from, or incomplete inhibition of EGFR tyrosine autophosphorylation sites in response to lapatinib, over time, led to a switch in the regulation of cell survival from HER2-HER3-PI3K signaling in lapatinib-naive HER2+ breast cancer cells, to EGFR-HER3-PI3K in cells that become resistance to lapatinib. Here, EGFR is linked to breast cancer.