As EGFR signaling can induce a tumor-suppressive microenvironment through upregulation of factors such as IL-6, TGF-β and progranulin, and induces PD-L1 expression, and PD-L1 can mediate resistance to TKIs through upregulation of YAP1, there is a clear preclinical rationale for the use of combination therapies simultaneously targeting PD-L1 and EGFR signaling (181). Here, EGFR is linked to neoplasm.