We demonstrated that proliferating tumor cells, either untreated tumor cells (Ki67+) or indolent tumor cells (Ki67+/low), were susceptible to immunoediting and escape during cell division, but quiescent tumor cells (Ki67−) failed to undergo immunoediting; in fact, they failed to up-regulate PD-L1 in the presence of IFN-γ stimulation. This evidence concerns the gene CD274 and neoplasm.