Chromosomal Jak translocations leading to constitutive activation of multiple oncogenic signaling pathways have been identified in hematological malignancies.19,20 In addition, activating mutations in Jak2 and Stat3 have been found in leukemias and solid cancers.21 In contrast, Stat1 is considered a tumor suppressor as it regulates expression of pro-apoptotic and anti-proliferative genes as well as molecules of the antigen presentation machinery, which increases tumor immunogenicity.22–24 A dual role of Jak-Stat signaling has also been observed in CRC. Here, SOAT1 is linked to neoplasm.