 In consequence, the RBM15-MLK1 fusion protein acts in an unregulated fashion to suppress MLK1 targeted genes while stimulating RPBJ target genes.This causes an over-active Notch signaling pathway and, among other abnormalities, expansion of fetal hematopoiesis and development of AMKL in a small percentage of adult mice.It is assumed that these events must be accompanied by other, as yet undefined, oncogenic (i.e., cancer causing) events to explain the development of human non-Down AMLK.