More intriguingly, the E167K variant in TM6SF2 seems able to disconnect the risk of NAFLD/NASH progression from cardiovascular risk, which is supported mainly by the Dongiovanni et al. study [142] showing that 188 (13%) out of 1201 subjects who underwent liver biopsy for suspected NASH were carriers of the E167K variant and that these carriers had lower serum lipid levels than noncarriers, more severe steatosis, necroinflammation, ballooning, and fibrosis and were more likely to have NASH and advanced fibrosis after adjusting for metabolic factors and the PNPLA3 I148M risk variant. Here, PNPLA3 is linked to steatosis.