Interestingly, phosphorylation levels of STAT5α were constitutively high and were further increased in the presence of IL-3, while presence of GNF-2 or GNF-2/AKI reduced pSTA5α to the levels obtained in the absence of IL-3, arguing that STAT5α phosphorylation is mediated mainly by Bcr-Abl and is less dependent on JAK2 activation, and suggesting that GNF-2 and AKIs are not direct inhibitors of STAT5α. Here, STAT5A is linked to acute kidney injury.