RAET1L and neoplasm: Nonetheless, these results suggest that sULBP6 and/or chronic NKG2D stimulation (54) by membrane-associated ULBP6 derived from ULBP6 overexpression may counteract the immune-activating effects of membrane-anchored NKG2DLs, resulting in NK cell dysfunction (52) and an immunosuppressive tumor microenvironment.