Previous studies have shown that the B55α subunit is upregulated in response to FTY720 treatment in AML patients with c-kit mutation [25] and cells with RNAi mediated knockdown of B55α expression are less responsive to FTY720 treatment [26] suggesting a role for B55α in tumor response to this potential chemotherapeutic. This evidence concerns the gene PPP2R2A and acute myeloid leukemia.