On the other hand, it is suggested that the aggravation of NASH in the CDAA-HF-T(−) group may be due to the proapoptotic hepatic microenvironment, introduced by the partial inhibition of the NF-κB phosphorylation and the overexpression of SULTE1E1. This evidence concerns the gene NFKB1 and metabolic dysfunction-associated steatohepatitis.