Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis

, © Silva et al. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and redistribution in any medium, provided that the original author and source are credited. The manuscript titled “Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis” aims to determine if there is a role for Hipk in JAK/STAT signaling. The novelty of this paper lies in the fact that hipk has been reported to have a role in several different pathways, but not yet in JAK/STAT signaling. The authors used several techniques to show that hipk overexpression in flies causes pigmented masses derived from hemocytes. They also showed that loss of hipk improves tumorigenesis outcomes in flies with the hop Tum-1 mutation, a mutation previously reported to be associated with increased JAK/STAT signaling. Lastly, the paper shows that hipk activates JAK/STAT signaling downstream of upd and interacts with Stat92E, the transcription factor of the pathway in flies. Collectively, the paper provides strong evidence to support the claim that hipk has a role in JAK/STAT signaling and should be further investigated as a potential therapeutic target for hemocyte derived human cancers. However, to help the reader better interpret the data, some clarifications and experiments could be addressed.