In this study we instead show that GCSF-induced upregulation of endogenous KIT occurs in a) undifferentiated 32D myeloblasts expressing wild type RUNX1, with the potential of maturing into differentiated granulocytes as well as in b) undifferentiated 32D myeloblasts expressing the RUNX1-MTG8 (also AML1-ETO or RUNX1T1-RUNX1, and here abbreviated as RM8) which are capable only of continuous growth, as it happens in the t(8;21)(q22;q22) acute myelogenous leukemia (AML). The gene discussed is RUNX1; the disease is acute myeloid leukemia.