In this article, Melo-Cardenas et al investigate the role of IL-13/IL-4 signaling in myelofibrosis and suggest that it plays a crucial role in driving fibrotic progression through megakaryocyte expansion and increased TGF-beta production.
In this issue of Blood, Melo-Cardenas et al explore the role of interleukin-13 (IL-13)/IL-4 signaling in myelofibrosis as an important pathway driving fibrotic progression through megakaryocyte expansion and increased transforming growth factor-beta (TGF-beta) production.(1)
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