Another interesting finding is the activation of JNK after WD in WT mice in both models, while JNK phosphorylation was significantly reduced in the NAFLD model after loss of Plin5. Taking into account that JNK mediates steatosis and glucose intolerance, this finding makes PLIN5 a clinically relevant target [48]. The gene discussed is PLIN5; the disease is metabolic dysfunction-associated steatotic liver disease.