Some studies reported that SAT exhibits increased expression of proinflammatory genes in patients with MO [5,6]; similarly, Plessis et al. demonstrated the significance of the SAT gene set in both the early stage of NAFLD and its progression to NASH [25], which may support the hypothesis that OLFM2 in SAT could play a role in NAFLD progression in the same way that OLFM2 affects the liver. Here, OLFM2 is linked to metabolic dysfunction-associated steatotic liver disease.