Alternatively, PPARα may have a role in regulating insulin sensitivity; it was recently shown that miR-34a inhibition ameliorates NASH by targeting the PPARα/AMPK pathway, thus regulating insulin signaling and steatosis.33 Altogether, restoring mitochondrial function appears to be key in counteracting metabolic overload and reinstating insulin signaling. This evidence concerns the gene INS and metabolic dysfunction-associated steatohepatitis.