The JAK‐STAT inhibitor tofacitinib blocks the IFNγ‐induced transformation from an NK cell‐sensitive phenotype to an NK cell‐resistant one in IFNγ‐reacted LC‐2/ad cells, thereby implicating that tofacitinib may be a promising agent to overcome IFNγ‐induced tumor immune escape, although it could be adapted to the limited number of NSCLC patients. The gene discussed is SOAT1; the disease is non-small cell lung carcinoma.