While the first generation RTKIs reversibly bind to EGFR with strong affinity for both, wild-type and the tumor-associated mutated receptor (L858R), the second generation RTKI afatinib also binds with high affinity to wild-type and mutated EGFR (L858R and T790M), however, this binding is irreversible [21,22]. This evidence concerns the gene EGFR and neoplasm.