Many genes involved in APL have similar cellular functions, but lack recurrence and consistency, except for FLT3, WT1, and KRAS. The physical and functional interactions of the mutated genes have been useful to discover driver mutations in cancers, the damage of these genes in APL is weaker than the interaction between mutant genes and different functionally related classes (15). This evidence concerns the gene FLT3 and acute promyelocytic leukemia.