The hypothesis retraces the CD34+ release from BM found in myelofibrosis (and also in MM patients) [48], driven by an up-take in intracellular calcium and/or calcium-containing matrix vesicle segregation—with consequent low calcium levels—inducing calcium-mediated signals of chemotaxis, here related to CMMC release in the blood stream [49]. This evidence concerns the gene CD34 and Miyoshi myopathy.