However, excessive MET expression can bypass the effect of EGFR inhibitors by directly interacting with these kinases and activating them, thereby counteracting the anti-tumorigenic effect of EGFR inhibitors.313 This finding illustrates that the aberrant protein interactions, which arise from the excessive proteins due to stoichiometry imbalance, could serve as a mechanism through which aneuploidy reshapes the interactome, thereby promoting tumorigenesis in tumor cells. The gene discussed is EGFR; the disease is neoplasm.