PCSK9 and metabolic syndrome: The findings are of importance for the understanding of the pathogenetic mechanisms underlying DPN in T2D because the long-term dyslipidemia outcomes seen in humans cannot be properly reproduced in rodents owing to substantial differences in lipid metabolism.33 In light of emerging therapies for dyslipidemia in T2D, such as PCSK9 inhibitors that promote a more aggressive lowering of serum cholesterol levels, our results suggest that current clinical trials including patients with very low serum cholesterol levels should pay close attention to signs of neuropathic damage.16