This requires not only homing and engraftment potential to the murine microenvironment but ability to express the phenotype of the original AML in terms of surface phenotype and of clonal markers such as chromosome translocations or deletions or of other abnormal molecular markers such as nucleophosmin-1, Flt3–ITD expression, or Ras mutations. This evidence concerns the gene FLT3 and acute myeloid leukemia.