This leads to an increase in IL‐4 expression and secretion, further promoting macrophage M2 polarization and triggering immune escape.[322] Interestingly, epiregulin (EREG) secreted by macrophages promotes EGFR‐TKI resistance via EGFR/ErbB2 heterodimer.[323] But in the scRNA sequencing data of the early stage of lung adenocarcinoma (LUAD) harboring EGFR mutations, TAMs are not polarized to a distinct state of either M1 or M2.[324]. The gene discussed is EGFR; the disease is lung adenocarcinoma.