First, it may be that the IFNγ produced during the normal antitumor response of pre-mNK cells upregulates PD-L1 on the tumor or other cells in a mechanism of adaptive resistance.65 Thus, when recently activated PD-1+CD4+ T cells come into contact with PD-L1+ cells, their antitumor activity will be suppressed. The gene discussed is IFNG; the disease is neoplasm.