We recently showed that development of acquired therapeutic resistance to the reversible HER2 and EGFR tyrosine kinase inhibitor lapatinib in HER2+ breast cancer cells can be mediated by a number of mechanisms including: (i) a switch in the regulation of cell survival from HER2-HER3-PI3K signaling in treatment naïve cells to EGFR-HER3-PI3K in resistant cells [16]; and (ii) expression of a truncated ErbB2 form preferentially expressed in tumor cell nuclei [17]. The gene discussed is EGFR; the disease is neoplasm.