In the present study, the circumvention of gefitinib resistanceby the newly identified HDACI candidate (flunarizine) was tested inhuman NSCLC cell lines displaying a range of key gefitinib resistancemechanisms (secondary EGFR T790 M (in H1975), KRAS mutation (in A549),PTEN loss (in H1650), and MET amplification (in H820)).Flunarizine is a selective calcium channel blocker with a histamineH1 blocking activity. This evidence concerns the gene KRAS and non-small cell lung carcinoma.