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. The gene discussed is INS; the disease is steatosis.