As flunarizine produced the mostremarkable increase in AcH3 amongthe positive HDAC-inhibiting drug candidates, it was selected fordetailed study in gefitinib-resistant NSCLC cell lines with differentresistance mechanisms (H1975-EGFR T790M; A549-KRAS G12S; H1650-PTENloss; H820-EGFR T790M; and MET amplification) (Table 3B). Here, KRAS is linked to non-small cell lung carcinoma.