This finding was further confirmed in other renal fibrosis models, such as polycystic kidney disease and UUO nephropathy.36,37 As mentioned previously, activating EGF/EGFR signaling appears to be a promising strategy for treating AKI and recovery after AKI.38 However, it is noteworthy that sustained activation of EGFR is associated with cell cycle arrest at the G2/M phase, leading to renal fibrogenesis after AKI.39,40 Therefore, exogenous EGF or HB-EGF may not be suitable for long-term treatment. This evidence concerns the gene HBEGF and acute kidney injury.