In addition, feniconazole nitrate has been identified as having potential in regulating phosphorylation changes with NAFLD and has been reported to alleviate the condition by activating facilitated glucose transporter member 4 (GLUT4) via the promotion of AKT phosphorylation at the Ser473 site and by blocking PPARγ phosphorylation at the Ser273 site mediated by cyclin-dependent kinases 5 (CDK5), thereby eventually decreasing the expression of adipogenic genes such as ACC. Here, CDK5 is linked to metabolic dysfunction-associated steatotic liver disease.