GK and metabolic dysfunction-associated steatotic liver disease: Based on evidence from genetics, biology, and drug development, excessive activation of hepatic GK may be detrimental to glucose and lipid metabolism: (I) constant activation of hepatic GK may lead to progressive deterioration of GK function, resulting in abnormal glucose metabolism; and (II) excessive glucose uptake stimulates lipogenesis through multiple pathways, leading to the development and progression of NAFLD.