As the onset of the pro-inflammatory tumor microenvironment has been shown to be synonymous with the increased infiltration of immune cells such as T lymphocytes into the tissue, CD16+ subsets of which can mediate ADCC (228), with both AMG510 (227) and MRTX849 (229), combining KRAS G12C inhibitors with anti-EGFR antibodies, which stimulate ADCC, may have synergistic effects in these tumors. Here, EGFR is linked to neoplasm.