CCL22 regulates Treg migration via binding to its receptor CCR4.[303] In EGFRmut lung adenocarcinoma, EGFR signaling upregulates the expression of CCL22 by activating cJun/cJun N‐terminal kinase, thereby promoting tumor cell recruitment of Tregs and forming an immunosuppressive microenvironment.[212, 230] EGFR activation was also found to promote the expression of CCL22 in human immortalized keratinocytes (HaCaT).[304]. The gene discussed is JUN; the disease is neoplasm.