APTR and metabolic dysfunction-associated steatotic liver disease: Despite this discrepancy, the replication of findings between CCl4-treated animals and patients with hepatic fibrosis (albeit of undisclosed etiologies) in a number of studies (Table 1) suggest that at least some lncRNAs identified in the CCl4 mouse model, namely, Aptr, Malat1, Neat1, and Hotair, may also be relevant to NAFLD fibrosis in humans.