Finally, repression of Aldh1a2/ALDH1A2 in PECs in both a murine CKD model (Figure 3A) and in patients with CKD (Figure 4C) is in stark contrast with enhanced Aldh1a2 expression in PECs and fibroblasts in mice with AKI induced by ischemia-reperfusion, peaking at 12 h and 2 days, and remaining elevated 6 weeks after ischemia-reperfusion, when kidney functions have returned to normal [11]. Here, ALDH1A2 is linked to chronic kidney disease.