RUNX1 regulates myeloid differentiation by modulating the extent of KIT-induced proliferation. In the presence of a functional RUNX1-miRNA mechanism, cells respond to myeloid differentiation stimuli, such as G-CSF (left). Increasing KIT-mediated proliferation, even in the absence of factors interfering with RUNX1, is sufficient to delay myeloid differentiation (middle). In the presence of factors that impair the RUNX1-miRNA mechanism (e.g. CBF fusion proteins or miRNAs targeting RUNX1-3′UTR), the effect of KIT-mediated proliferation reinforces the effects of deregulation of miRNAs controlled by RUNX1 and involved in differentiation (e.g. miR-223), thus resulting in complete block of myeloid differentiation (right).