The release of NKG2D-L from the cell surface in their soluble form (sNKG2D-L) could have at least three consequences: a reduction in NKG2D-L density at the tumor cell surface, blocking of the NKG2D-binding site and, finally, internalization and downmodulation of the NKG2D receptor on effector cells upon persistent engagement of the sNKG2D-L (Salih et al., 2008; Ashiru et al., 2010). The gene discussed is KLRK1; the disease is neoplasm.