Importantly, we have previously shown that the interaction between Ang II/AT1R and DPP4 is pivotal in the pathophysiology of kidney diseases, with DPP4 inhibition preventing glomerular and tubulointerstitial injury, proteinuria, oxidative stress, inflammation, and fibrosis [24, 56, 57, 58] processes that are at least partially driven by Ang II/AT1R signaling. This evidence concerns the gene DPP4 and kidney disorder.