Our analyses of mutant EGFR recycling in the context of Src were based on prior evidence that Src-dependent signaling is critical for EGFR-mediated oncogenesis; this has been established in vitro using Src inhibitors as well as mutational approaches [7], and Src is overexpressed or hyperactive in NSCLC as well as other cancers where EGFR mutations or overexpression have been implicated in oncogenesis [9,10]. The gene discussed is EGFR; the disease is cancer.