Recently, Galan-Díez et al. [148] postulated that at the onset of AML, osteoblasts seem to perform a dual function: they seem to exert protective signals of an elusive nature and, at the same time, AML blasts subvert serotonin receptor signalling in mature osteoblasts through the kynurenine–HTR1B–SAA–IDO1 axis to persist within the endosteal niche. Here, HTR1B is linked to acute myeloid leukemia.