The HFD-treated Ldlr−/−.Leiden mouse is sensitive to targets playing a role in human NASH including caspase-1 inhibitors, diglyceride acyltransferase (DGAT) inhibitors, sodium dependent bile acid transport inhibitors [10,16,44], as well as nutritional components such as butyrate, propionate, probiotica, and protein hydrolysates [13,45], but further validation studies of the model by evaluating the response with other NASH candidate drugs or established compounds in the future are warranted. The gene discussed is CASP1; the disease is metabolic dysfunction-associated steatohepatitis.