While additional studies will be necessary to delineate the relationship between MALAT1 and CXCL5 and determine the contribution from different cell types in the liver to the MALAT1-CXCL5 pathway, these findings preliminarily suggest that functionally relevant differences in MALAT1 expression may contribute to the development of NAFLD fibrosis through mechanisms involving inflammatory chemokines. This evidence concerns the gene CXCL5 and metabolic dysfunction-associated steatotic liver disease.