Much worse, after treatment with inhibitors, cancer cells frequently acquire secondary mutations within the target protein, rendering the interface of the active pocket to reduce drug affinity (e.g., Ibrutinib-resistant C481S mutation of Bruton tyrosine kinase (BTK) in chronic lymphocytic leukemia (CLL) [34,35,36,37,38] and osimertinib-resistant C797S mutation of EGFR in NSCLC [39,40,41,42]). This evidence concerns the gene EGFR and cancer.