Further mechanistic studies underscored a new dynein-driven mechanism of diabetic podocytopathy, in which synchronous upregulation of dynein subunits in response to hyperglycemia results in enhanced dynein-mediated mistrafficking and dyshomeostasis of nephrin, leading to podocyte injury.10 Investigating how diabetic stresses drive the upregulation of dynein will help us dissect potential therapeutic targets to remodel the pathogenesis of DN. Here, NPHS1 is linked to liver dysplastic nodule.