KIT is a member of the type III RTK family, and ligand-independent activation of KIT can be caused by gain-of-function mutations that have been reported in core binding factor (CBF) leukemia, and AML subgroups with inv(16) and t(8; 21) [65-67], which result in expression of the abnormal fusion genes CBFβ/MYH11 and RUNX1/ETO, respectively. The gene discussed is RUNX1; the disease is leukemia.