Our study has some limitations that should be noticed and restrict the extrapolation of our results to the general population, such as: (a) the sample size may have limited the interpretation of the role that T2D and PNPLA3 p.I148M and TM6SF2 p.E167K polymorphisms play in the development of advanced fibrosis; (b) T2D patients were predominant in the NASH cohort and may have disturbed the results regarding the effect of both polymorphisms in advanced fibrosis in the absence of diabetes. The gene discussed is TM6SF2; the disease is metabolic dysfunction-associated steatohepatitis.