Nevertheless, like GJs, EVs can also contribute to escaping anti-tumor immune defense mechanisms, for instance by “flooding” the natural killer (NK) cells’ receptor NKG2D with EV-transported ligands, which results in receptor downregulation and impairment of the cytotoxic function of the immune cells [401], or by transporting Fas ligands (FasL) to trigger Fas-dependent apoptosis [402,403,404]. This evidence concerns the gene FASLG and neoplasm.