We previously reported that ARAP1 could maintain persistent EGFR activation by reducing the ubiquitination of EGFR through interacting with CIN85 and that ARAP1-AS2 directly interacted with ARAP1 and promoted ARAP1 expression and then regulated CIN85 indirectly in HK-2 cells (Li et al., 2020b); however, the mechanism of persistent EGFR activation in other renal cell populations and animal models of DKD is still unknown. Here, SH3KBP1 is linked to diabetic kidney disease.