As the role of IL-15 in NK cell metabolism is regulated by mTOR activation, inhibition of mTORC1 completely neutralized glycolysis and oxidative phosphorylation levels in the CIS-deficient iPSC-derived NK (iNK) cells compared with wild-type, demonstrating the mTOR pathway mediates the improved metabolic fitness and enhanced effector function. The gene discussed is IL15; the disease is in situ carcinoma.