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From an immunological perspective, these associations arise from a breakdown in self-tolerance mediated by overlapping T-cell and B-cell autoreactivity, shared cytokine pathways (e.g., IFN-, IL-18), and common antigen-presenting HLA alleles
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Studies in humans and animals with non-alcoholic fatty liver disease show that CD44 plays a key role in the inflammation and liver damage in NAFLD.[ref] Other genetic studies have looked at genes in pathways known to be involved in acetaminophen metabolism, including genes related to sulfation, glucuronidation, and glutathione production
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