Additionally, our data might point to roles for both ligands in the escape from immunosurveillance by tumor cells: sustained over-expression of MICA at the cell surface of HPV-positive cells, which could promote downregulation of the NK cell functions; and the shedding of MICB in HPV-negative cervical cancer cells, which could bind to NKG2D receptors and outcompete cell-surface activating ligands. This evidence concerns the gene MICB and neoplasm.