We hypothesize that this switch in splicing contributed to the therapeutic phenotype induced by DIAVIT, including preventing increases in albuminuria and glomerular water permeability (Fig 1), glomerular fibrosis (Fig 2), and the ultra-structural changes to the mesangial cells, endothelial cells, GBM, and podocyte foot processes (Fig 4), which have previously been shown to be rescued by VEGF-A165b treatment in models of DN and kidney disease [7,12]. This evidence concerns the gene VEGFA and liver dysplastic nodule.