AML cells exploit further signaling axes of the TNF/TNFR superfamily, such as the 4-1BB-ligand/4-1BB (CD137L-CD137) pathway and the receptor activator of nuclear factor kappa B (RANK)-ligand RANK pathway (106, 107) to inhibit the immune system in a similar way as described for GITR. The gene discussed is TNFRSF11A; the disease is acute myeloid leukemia.