We generated BRAFi‐resistant variants from four established BRAFV600E and two freshly explanted human melanoma cell lines in vitro and measured: their susceptibility to lysis mediated by IL‐2 activated NK cells from healthy donors; expression of NK‐cell receptor ligands and HLA class I antigen processing machinery (APM) components in melanoma cells before and after acquisition of resistance to BRAFi vemurafenib or dabrafenib and effects of BRAFi on NK cells. The gene discussed is IL2; the disease is melanoma.