EGFR and neoplasm: However, their clinical efficacy is limited by various factors, such as the presence of activating mutations of the EGFR downstream signaling pathway (e.g., RAS mutations), which result in the constitutive activation of the pathway regardless of ligand binding [21,22,23], the tumor microenvironment (TME), which can restrict antibody penetrance and NK cell migration into the tumor, and/or the presence of certain modulatory non-coding RNAs that hamper the negative modulation of the Wnt signaling pathway leading to EGFR-mAb resistance [20].