Interestingly, within 1 h of treatment with either drug the phosphorylated EGFR and total EGFR have increased in P848L‐expressing cells, but with no significant change observed in L858R mutants, which is in accordance with the previous findings of increased EGFR signaling by JAK2 inhibition in established TKI‐resistant NSCLC cells in vitro and in primary tumors due to the surface abundance of EGFR 41. This evidence concerns the gene JAK2 and non-small cell lung carcinoma.