EGFR and neoplasm: Among them, active dimer sub‐units within ligand‐free oligomers are the high‐affinity binding sites to promote tumor growth.[58] Several mechanisms can disrupt the stringent control of EGFR signaling, such as increased ligand production, overproduction of EGFR protein, mutations that result in the continuous activation of EGFR, impaired downregulation of EGFR, and the activation of EGFR via interactions with other cell‐surface receptors.[59] In this review, we mainly focused on the overproduction of EGFR and mutations causing constitutive activation of EGFR.