Another interesting example is the one offered by the study of Choi et al. [153] in which they not only show the participation of CK2 in inflammatory pathologies, such as obesity and NAFLD, but also identify the obesity-linked Ser-164 phosphorylation of SIRT1 by CK2 as the main responsible mechanism for inhibiting the nuclear localization of SIRT1 and for affecting, to some extent, its enzymatic activity. This evidence concerns the gene SIRT1 and metabolic dysfunction-associated steatotic liver disease.