However, as PCB-118 and β-HCH did not correlate with CYP1A2 expression and did not accumulate to liver in these studies [16, 43], and as decreased CYP1A2 protein expression levels were observed in liver microsomes of patients with NASH [44], possible hepatic accumulation should take place by other mechanisms. Here, CYP1A2 is linked to metabolic dysfunction-associated steatohepatitis.