Suboptimal 5-Aza dosage might have influenced this result, although our observation of an actual loss of IFN-γ+ Th1 cells would argue against this hypothesis and for a targeted shift in T-helper differentiation. In vivo experiments in mice and first reports in humans further support the suppressive properties of 5-Aza on CD4+ T-cells, in which 5-Aza treatment was sufficient for engraftment and prevented GvHD occurrence [13, 31]. The gene discussed is IFNG; the disease is graft versus host disease.