Importantly, the authors observed that overexpression of full-length RUNX1b isoform repressed TIMP1 promoter activity, whereas the truncated RUNX1a isoform and RUNX2 exerted the opposite effect, raising the possibility that a deregulation in RUNX1 splicing, rather than its overexpression, could contribute to a higher NAFLD prevalence in children with Trisomy 21. This evidence concerns the gene RUNX1 and metabolic dysfunction-associated steatotic liver disease.