Therefore, these results collectively suggest a causal role of impaired ketogenesis, specifically Hmgcs2 deficiency, in the development of fatty liver disease in postnatal mice, analogous to the rare inborn mitochondrial HMGCS2 (mHS) deficiency disorder, in which infants frequently present with fatty liver [[29], [30], [31], [32]]. Here, HMGCS2 is linked to Hepatic steatosis.