Hence, on the basis of the results of our study, it is also possible to hypothesize that the presence of NAFLD and coexisting clinically significant fibrosis might partly contribute to glycaemic worsening, possibly through exacerbation of systemic and hepatic insulin resistance, and increased production of multiple hepatokines (such as, for example, fetuin A, fetuin B or fibroblast growth factor-21) and proinflammatory cytokines (such as, for example, tumour necrosis factor-α or interleukin-6) [4,6,9]. This evidence concerns the gene FETUB and metabolic dysfunction-associated steatotic liver disease.