The renin–angiotensin system (RAS) is a major regulator of renal fibrosis. Besides the classical renin/Angiotensin-converting enzyme 2 (ACE2)/angiotensin II (Ang II)/AT1 and AT2 axis, multiple new axes have been recently described. The new members have added new dimensions to RAS, including the ACE2/ANG (1–7)/Mas receptor axis, the prorenin/(pro)renin receptor(PRR)/intracelluar pathway axis, and the Angiotensin A (Ang A), alamandine-Mas-related G protein coupled receptor D(MrgD) axis. This review summarized recent studies regarding role of the non-classical RAS axis in renal fibrosis, and its possible implications to the intervention of progression of chronic kidney disease.