“…4 Biological functional consequences of this RUNX1a-dependent inhibitory effect have since been extensively investigated in the field, particularly in the areas of HSCs and leukemia. 5,6 Through such endeavors over the past two decades, a significant body of knowledge has been accumulated, and we now know that the two FL forms, RUNX1b and RUNX1c, act as negative regulators for HSC pool size, and RUNX1a functions as a positive regulator (see figure). Fine-tuning of the balance between these positive and negative regulators transcribed from a single hematopoietic gene, RUNX1, is clearly shown to be one of the critical mechanisms in determining HSC population size.…”