Tumor-associated macrophage interaction through the EREG/EFGR pathway induces resistance to tyrosine kinase inhibitors in patients with LAUD,[32] while EGFR mutations have been found to lead to EREG overexpression through activation of the MEK/ERK pathway,[33] whereas 30% to 50% of patients with lung adenocarcinoma possessed mutations in the EGFR gene. Here, EREG is linked to neoplasm.