Given that copper and lipids are independently associated with dyslipidemic disease pathogenesis (Blades et al., 2021), and excess serum copper has been significantly associated with the risk of NAFLD (Chen et al., 2021c; Lan et al., 2021), along with KC counteraction of copper-fructose-induced hepatic steatosis (Song et al., 2018), further in vivo and in vitro experiments related to copper metabolism should be conducted to investigate the influence of copper metabolism on the role of KCs in NAFLD. The gene discussed is CALCA; the disease is metabolic dysfunction-associated steatotic liver disease.