Signal transduction pathways are crucial for coordinated development and growth of multicellular organisms. Dysregulation and mutations of components in these pathways can often lead to tumourigenesis. The evolutionarily conserved Homeodomain-Interacting-Protein-Kinase (Hipk) is a potent growth regulator and elevated levels of Hipk in Drosophila lead to tumour-like masses resembling those found with activated JAK/STAT signaling. A point mutation similar to those seen in human blood cancers in the Drosophila Janus kinase (called hop) causes constitutive activation of the JAK/STAT pathway and results in blood cell tumours in larval and adult stages. We investigated whether Hipk causes tumours through JAK/STAT. First we show that elevated Hipk in blood cells phenocopies effects seen with the hyperactive form of Hop. Furthermore, Hipk induces enhanced proliferation of hemocytes. We find that reduction of Hipk can suppress the tumorigenic effects of activated Hop. RNAi against Hipk in hemocytes can suppress both the timing of lethality and the tumour load in activated hop flies. Furthermore, we find that Hipk is required for endogenous JAK/STAT pathway activity, since homozygous mutant tissue shows markedly reduced expression of a STAT reporter. To investigate the mechanism underlying this interaction, we performed a proximity ligation assay (PLA) between Hipk and STAT92E, the Drosophila STAT. Cells co-expressing Hipk and STAT92E show a robust PLA signal indicating an interaction. We are currently confirming this through in vitro and in vivo binding studies. Our work shows that Hipk is required for JAK/STAT signaling during normal development and in fly blood cancer.