For instance, the anti-EGFR CL4 aptamer exerts a strong apoptotic effect on human NSCLC [75], blocks the invasiveness of GBM cells expressing either the EGFRwt or EGFRvIII mutant [76,77] and prevents the EGFR/integrin αvβ3 interaction on the surface of TNBC cells with a mesenchymal stem-like phenotype, which we first found to be required for vasculogenic mimicry and tumor growth of aggressive and poorly differentiated TNBC subtype [78,79]. This evidence concerns the gene EGFR and neoplasm.