Here, the establishment of a senescence program in persistent SnCs has been shown to subvert immune clearance through the activity of MMP-dependent shedding of selected NKG2D-Ls and suppression of NKG2D-mediated immunosurveillance [126–128] leading to SnCs persistence, as described in cancer epithelial cells and in residual tumors from patients with breast and prostate cancer who underwent genotoxic chemotherapy [127]. This evidence concerns the gene KLRK1 and cancer.