Furthermore, in addition to PAKs, PF-3758309 inhibited the activity of AMPK, CAMK2, CDKs, PKC and multiple tyrosine kinases, while increasing the activity of MTOR and MAPKs in AML primary blast, suggesting that potential mechanisms of acquired resistance involving these pro-survival and mitotic kinases may operate in primary cells. The gene discussed is PRKAA1; the disease is acute myeloid leukemia.