MICA and neoplasm: The so far described mechanisms included the down-regulation of activating (e.g. NKG2D) and up-regulation of inhibitory (Tim-3, LAG3, PD-1, ...) receptors or conversely, the shedding or down-expression of activating ligands (ULPB, MICA/B) and over-expression of inhibitory molecules (PD-L1, non MHC-class I ligands) by the tumor cells [31, 32].