This hypothesis is supported by several loss-of-function (Msx1, Rfx4 and Pax6) and gain-of-function (Adcyap1r1 and En1) mouse models of CH in which SCO development and/or function is severely compromised [8], [11], [12], [13], [16], [33]. The gene discussed is EN1; the disease is cyclic hematopoiesis.