A broad category including benign liver steatosis, non-alcoholic steatohepatitis, liver fibrosis, cirrhosis, and hepatocellular cancer is non-alcoholic fatty liver disease (NAFLD). Recent years have seen NAFLD emerge as a significant health concern. It has become a worldwide priority to find ways to stop or slow the development of NAFLD. Even though there are a number of medicinal therapies for NAFLD that are undergoing clinical trials, changing one's lifestyle continues to be the most important part of treatment. Agents such as dapagliflozin, which are sodium-glucose co-transporter type-2 inhibitors (SGLT-2i), are showing great promise. Apoptosis, low-grade inflammation, autophagy, and processes regulated by SGLT-2i, including the endoplasmic reticulum (ER), are all involved in the pathophysiology of NAFLD. We provide the present state of knowledge on the pathophysiology of NAFLD in this review, with an emphasis on the possible role of SGLT-2i in the onset and progression of NAFLD, supported by the best available evidence from in vitro and animal research. Considering this information, doing additional mechanistic studies would enhance our comprehension of the specific pathways contributing to the development of NAFLD and the possible positive effects of SGLT-2i when used to treat NAFLD.