found that AREG secreted by cancer cells could bind to Tregs and activate EGFR signaling, which regulates posttranslational modification of Foxp3 protein through glycogen synthase kinase‐3 beta (GSK‐3β), enhancing the immunosuppressive function of Treg cells.[372] And AREG/EGFR axis has also been identified as a potential therapeutic target in lupus nephritis, where it downregulates pathogenic CD4+ T helper cell responses.[373] Compared to EGFR‐negative Tregs, EGFR‐positive Tregs exhibit greater immunosuppressive capabilities. Here, EGFR is linked to lupus nephritis.