HSCT-derived immune derangement has been found to trigger bone loss, most frequently in allogeneic HSCT recipients, compared to autologous HSCT, due to the increased synthesis of specific inhibitors of the canonical Wnt/Beta Catenin pathway, Dickkopf-1, and Sclerostin (176), principally as a consequence of GVHD and/or administration of GVHD prophylactic treatments. The gene discussed is SOST; the disease is graft versus host disease.