EGFR and neoplasm: Our analysis revealed that P848L (a) does not bind erlotinib; (b) is turned over less rapidly than L858R (a common tumor‐derived EGFR mutation); (c) is not autophosphorylated at Tyr 1045 [the major docking site for Cbl proto‐oncogene (c‐Cbl) binding]; and (d) does not bind c‐Cbl.