In contrast, in strictly identical experimental conditions, HFD-fed BALB/c mice did not show evidence of liver triglyceride accumulation and were devoid of NAFLD, even though levels of ALT and AST were increased in both strains in response to HFD [13], suggesting the involvement of genetically driven mechanisms of resistance to diet induced NAFLD in BALB/c mice. The gene discussed is GPT; the disease is metabolic dysfunction-associated steatotic liver disease.