IL-6 activates various signaling pathways, including the JAK/STAT, PI3K/AKT/MTOR (also a main pathway downstream to antigen-recognizing T cell receptors (TCRs)) and MAPK/ERK pathways [14], but JAK/STAT signaling seems responsible for most IL-6 effects in GVHD since STAT3 activation induces the development of alloreactive Th17 cells and suppresses the development of inhibitory Tregs [15,16,17]. The gene discussed is SOAT1; the disease is graft versus host disease.