Moreover, TLR2 deficient mice on a dietary-induced NASH did not develop steatohepatitis and displayed a lower expression of pro-inflammatory cytokines compared to wild type animals [12], and, furthermore, as recently shown, TLR2 can activate the inflammasome in Kupffer cells, leading to pro-inflammatory cytokine production and NASH development in mice models [13]. Here, TLR2 is linked to metabolic dysfunction-associated steatohepatitis.