Mice with early nephritis from NNMT-KO had significantly lower levels of IL-1b and F4/80-positive cells and increased SIRT1 and SIRT7, inhibiting tissue inflammation via NF-κB, suggesting that SIRT1-mediated NF-κB deacetylation participates in the mechanism by which NNMT inhibition improves fibrosis [130]. Here, SIRT1 is linked to nephritis.