In conclusion, there are substantial data strongly suggesting that the activation of the PTTG1/DLK1 axis is a key factor involved in the pathophysiology of NAFLD, liver fibrosis, and liver cancer, which, in turn, raises the hypothesis that disruption of this signaling pathway could be of therapeutic utility in these pathological conditions. This evidence concerns the gene PTTG1 and metabolic dysfunction-associated steatotic liver disease.