Notably, our observations revealed a new mechanism whereby treatment with MIYAIRI 588 designates the AMPK activation as a starting point and regulates different pathophysiological events, such as lipid and energy metabolism, insulin sensitivity, and oxidative stress response, through consistent and systematic signaling pathways, thereby causing pronounced suppression of NAFLD progression (Figure 10). The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.