ARTD9 may also be directly involved in editing or inhibiting the IFNγ-dependent host immune response against HR-subtype DLBCL either through its transcriptional co-repressor activity and termination of IFNγ-mediated gene expression and inhibition of the extrinsic IFNγ-induced anti-proliferative and pro-apoptotic STAT1-IRF1-TP53 axes or through its transcriptional co-activator activity and induction of expression of the NK/T-cell inhibitory molecules i.e., PD-1L and increasing the resistance of IFNγ-treated tumor cells towards NK cell- or lymphokine activated killer-mediated lysis [470]. This evidence concerns the gene IRF1 and neoplasm.