We speculate that the observed phenotype of DKO mice is likely a consequence of Pnpla3 deletion and depends on the activation of alternative signaling pathways triggered by accumulation of certain saturated FAs species in the concomitant absence of Pnpla3 and Mgl. In addition, since PNPLA3 was observed to have maximal hydrolytic activity against TG, DG, and MG with a strong preference for oleic acid as the acyl moiety [10,13], we corroborate that these lipid classes would accumulate in the liver driving macro- or microvesicular steatosis. The gene discussed is PNPLA3; the disease is steatosis.