In particular, excess fatty acid delivered to the liver from blood following dysregulated lipolysis in adipose tissue could lead to the activation of c-Jun N-terminal kinase-activator protein-1 and inhibitor of NF-κB kinase-NF-κB inflammatory pathways, which are critically involved in the development of the chronic inflammatory state in NAFLD (Cai et al., 2005; Hotamisligil, 2006; Buzzetti et al., 2016). Here, NFKB1 is linked to metabolic dysfunction-associated steatotic liver disease.