For example, the levels of plasmin-activator inhibitor are increased in patients with diabetes type 2; thus, plasmin-mediated post-translational cleavage of the VEGF-A 189 isoform could be dysregulated in the kidneys of patients with DN.[24, 25] This dysregulation would lead to a decrease in the cleavage products of VEGF-A 189, which may play a role during disease phases with decreased angiogenic potential.[18]. This evidence concerns the gene VEGFA and liver dysplastic nodule.