For example, after cleavage by caspase-1 at Asp64, PPARγ translocates to mitochondria, leading to attenuation of medium-chain acyl-CoA dehydrogenase (MCAD) activity and inhibition of fatty acid oxidation, which brings about the accumulation of lipid droplets and differentiation of tumor-associated macrophages (TAMs), thus resulting in an ultimate suppression of tumor growth [53, 54]. The gene discussed is ACADM; the disease is neoplasm.