A possible explanation was that, early post-APBHSCT, continuous cytotoxic activity against myeloma cells is driven by the activating signals of natural killer cells to achieve complete remission, leading to downregulation of the these activating signals and increased expression of inhibitory receptors (NKG2A and KIR2DL1), confirming the characteristic phenotype terminally differentiated natural killer cells [48]. This evidence concerns the gene KLRC1 and plasma cell myeloma.