SL inhibited colocalization of NLRP3 and apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) as well as α-tubulin and acetylated-α-tubulin in response to palmitate treatment, explaining that the NAD+/SIRT2 pathway was an important mediator through which SL prevented NLRP3 inflammasome activation during NAFLD (Zhang et al., 2018). Here, NLRP3 is linked to metabolic dysfunction-associated steatotic liver disease.