The fact that neither Nlrp3 deletion/pharmacologic inhibition nor Casp1 deletion (which blocks the final common pathway for all inflammasomes) ameliorated any of the histologic features of NASH, suggests that at least in the HFHC-fed mouse model these features are not driven predominantly by inflammasome activation. Here, NLRP3 is linked to metabolic dysfunction-associated steatohepatitis.