EGFR and cancer: Known exon 19 deletion (del19), exon 21 (L858R) substitution mutation causing excessive activation, T790M, C797S inducing resistance to targeted oncotherapy (7, 8), and the tyrosine kinase inhibitors (TKIs) that selectively bind to EGFR function as the most important therapeutic class for cancer targeted therapy, such as gefitinib, afatinib, and osimertinib.