To identify which ligands are responsible for the chronic activation of EGFR and consequent fibrosis, it was found that amphiregulin, a low-affinity ligand for EGFR whose expression is increased following an AKI, drives, amplifies, and integrates profibrotic signals in the proximal tubule cells and is crucial and adequate for AKI-induced fibrosis in mice in vivo (Kefaloyianni et al., 2019). Here, AREG is linked to acute kidney injury.