More recently, Galán-Díez et al. showed that AML cell proliferation depended on serotonin signaling in osteoblasts, where the oncometabolite kynurenine, a hallmark in MDS and AML patients, bound to the serotonin receptor 1B on osteoblasts and formed a vicious positive feedback loop through proinflammatory pathways.187 Taken together, the reversal and bone formation phases may contribute to chemosensitivity and self-renewal of leukemia cells. The gene discussed is HTR1B; the disease is acute myeloid leukemia.