Given that our ANN approach provides the probability of functional relationship–regardless of the activity status (up or downregulation)–and the current conflicting results in the literature, further studies in humans or in vivo are required to clarify these contradictions, although the current available evidence clearly supports an involvement, either by presence or absence, of RUNX1 in NAHLD and NASH. This evidence concerns the gene RUNX1 and metabolic dysfunction-associated steatohepatitis.