These include mechanisms of hemodynamics (hyperfiltration and the renin–angiotensin–aldosterone system (RAAS)), or in oxidative and substrate stress metabolism, and also the interaction of sex hormones with the signal transduction of TGF-β1 (transforming growth factor beta 1), the main mediator of DKD development and progression, is already known. This evidence concerns the gene TGFB1 and diabetic kidney disease.