This has been demonstrated to have both pro-inflammatory and immuno-regulatory actions,[39] importance in migration of Treg and conventional T cells to GVHD target organs,[40] and to mediate immune-regulatory function in FoxP3+ Tregs in experimental GVHD.[41] In keeping with published data in solid organ transplantation tolerance, TOL patients had decreased expression of anti-apoptotic (DAPK1, SOD2, PPT1, SOCS2, VNN1, SMAD1, GSN), and increased expression of pro-apoptotic (GZMH, PLEKHF1) mediators, as well as involvement of cell cycle control genes. The gene discussed is FOXP3; the disease is graft versus host disease.