Although the 12-week HFD is a model of early NAFLD, as showed by histology, we found a slight increase of the lncRNA CARMN that is a pro-inflammatory mediator that is upregulated in macrophages treated in vitro with high glucose and palmitic acid and in macrophages isolated from diabetic mice and whose transient overexpression stimulates the expression of inflammatory genes and of CD36 [23]. Here, CD36 is linked to metabolic dysfunction-associated steatotic liver disease.