STK39 and acute myeloid leukemia: Similar results were obtained in human AML cells, where ectopic expression of either constitutively active phosphomimetic mutant of OXSR1 (OXSR1T185E,S325E) or constitutively active phosphomimetic mutant of STK39 (STK39T233E,S373E) restored cell proliferation defects caused by the disruption of endogenous WNK1, but neither OXSR1WT nor STK39WT were able to do so (Fig. 2j and Supplementary Fig. 2i, j).