KLRK1 and neoplasm: Based on the demonstrated role of NKG2D signals in inducing NK activation favoring NK degranulation rather than adhesion to tumor cells [18] during ADCC, the induced trastuzumab activity after chemotherapy treatment observed in our model is likely due to the interaction between NKG2D ligands with their receptor, as supported by the ability of anti-NKG2D receptor antibodies to abrogate the chemotherapy-induced increase of in vitro trastuzumab-dependent ADCC.