Mutations on chromosomes 18 to 21 are considered EGFR-TKIs sensitive, while modifications on 20-T790M are not sensitive to EGFR-TKIs.[21] In around 1% of NSCLC patients, this mutation is hypothesized to include a threonine-methionine substitution in exon 20, boosting the mutant EGFR’s affinity to adenosine triphosphate competitively limiting the ability of reversible EGFR-TKIs to attach mutations on chromosomes 19 and 21 accounts for 90% of all modifications. This evidence concerns the gene EGFR and non-small cell lung carcinoma.