Interestingly, recent experimental research based on animal models conducted by Hadjihambi et al. [107] observed that genetically modified mice are haploinsufficient for monocarboxylate transporter-1 (MCT1)—a ubiquitous cotransporter of short-chain fatty acids, lactate, and ketone bodies with a proinflammatory role also involved in microglial activation—show a NAFLD-resistant phenotype despite obesogenic diet and adipose tissue accumulation, protecting from liver, cerebrovascular, glial and proinflammatory systemic alterations. The gene discussed is SLC16A1; the disease is metabolic dysfunction-associated steatotic liver disease.