In view of the causes of its drug resistance, some researchers explored its mechanism: TAMs in the TME secretes EREG (one of the ligands of EGFR), induces ERbB2 to form EGFR/ERbB2 heterodimer, downregulates cleaved caspase nine and other apoptotic proteins through its downstream PI3K/AKT pathway, inhibits the apoptosis of tumor cells, and then mediates the resistance of NSCLC to EGFR-TKI inhibitors [111]. Here, EGFR is linked to neoplasm.