Indeed, we observed that (i) ACC1-deficient iNKT cells demonstrated low FABP expression, (ii) exogenous fatty acid not only reversed the effects of ACC1 deficiency on glycolysis and apoptosis, it also restored the expression of both FABPs and PPARγ, and (iii) treating ACC1-deficient iNKT cells with exogenous palmitate or a PPARγ agonist and then transferring them into iNKT cell-deficient mice restored AHR in OVA- or HDM-induced asthma models. The gene discussed is AHR; the disease is asthma.