Whereas the main mechanism of this treatment in various other cancers is the reactivation of suppressed and exhausted cytotoxic CD8 T cells, this does not seem to be the case in HL.4 HRS cells in most cases of HL have lost expression of MHC class I, preventing their recognition by CD8 T cells.5 It is still unresolved whether the effects of anti-PD1 antibody treatment are mediated by effects on NK cells or on cytotoxic CD4+ T cells, or through a reverse, HRS cell-supporting signaling of PD-L1 into the HRS cells, or a combination of these factors. The gene discussed is CD8A; the disease is cancer.