CTNNB1 and graft versus host disease: 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.