EGFR and neoplasm: With respect to the Del19 and L858R mutations, first-generation TKIs, such as gefitinib and erlotinib, can competitively bind to the ATP binding site of the EGFR tyrosine kinase domain, inhibit its kinase activity and autophosphorylation, and block EGFR-mediated signal transduction, thus inhibiting tumor cell proliferation (Pao and Chmielecki, 2010; Roskoski, 2014).