It was reported that MICA and MICB can be proteolytically cleaved in senescent cells and hence allowed senescent cells to escape NK cell/macrophage-mediated immunosurveillance [160], which can be abolished by the antibody that targets the α3 domains of MICA/MICB and prevents their shedding, leading to tumor regression in the mouse models of melanoma and acute myeloid leukemia [161,162]. The gene discussed is MICB; the disease is neoplasm.