Among these lipids, cholesterol is abundantly produced from iNKT cells necessary for IFN-γ induction of lactic acid in the tumor microenvironment which reduces PPARγ expression in intra-tumoral iNKT cells, thereby reducing cholesterol synthesis and IFN-γ production, and restoring lipid synthesis by activating PPARγ and improving treatment efficacy on tumors [103]. The gene discussed is IFNG; the disease is neoplasm.