Pro-NASH stimuli increased the expression levels of KMT1B in liver in vitro and in vivo, while KMT1B deficiency allowed normal expression of Sirtuin (Sirt-1), which, in turn, inhibited the nuclear factor kappa B (NFkB)-dependent transcription of proinflammatory mediators [25]. This evidence concerns the gene SUV39H2 and metabolic dysfunction-associated steatohepatitis.