The variation between the gene expression changes seen between venetoclax and ruxolitinib therapy is important as IFNγ-dependent MHC-II expression in recipient tissues and subsequent activation of donor CD4+ T cells is now recognised as a key priming event in the onset of GVHD (22) and may explain, in part, why ruxolitinib + RIC treated recipients developed late skin GVHD. The gene discussed is CD4; the disease is graft versus host disease.