Recently it was found that ADAM17 has the ability to hydrolyze MICA/B on the surface of tumor cells to generate soluble MICA/B (sMICA/B) (52), the latter of which alters the conformation of NKG2D on the surface of NK cells (234) and affects the recognition and binding of membranous MICA with NKG2D, thereby inhibiting NK activation signals and reducing the killing sensitivity of NK cells to tumor cells (235). The gene discussed is ADAM17; the disease is neoplasm.