Moreover, another potential therapeutic target, miR-149, was shown to suppress the progression of NAFLD in an HFD-treated mouse model by downregulating the expression of inflammatory factors (TNF-alpha, IL-1beta, IL-6, and NF-kB) and apoptotic-related factors (caspase-12 and CHOP), thus, alleviating the ER stress-induced inflammation and apoptosis by inhibiting the activating transcription factor 6 α (ATF6) signaling pathway [152]. The gene discussed is ATF6; the disease is metabolic dysfunction-associated steatotic liver disease.