While the truncal activating mutations in EGFR provide high-response rates to the targeted EGFR TKIs, these responses are often short-lived27,28 unlike those to Imatinib in BCR-ABL1 fusion driven chronic myeloid leukemia (CML)46,47. This evidence concerns the gene EGFR and chronic myelogenous leukemia, BCR-ABL1 positive.