GI tumor cells can release metabolites such as kynurenine, which activate the aryl hydrocarbon receptor (AhR)–RUNX1 axis in hematopoietic progenitors, skewing their differentiation toward megakaryocytes at the expense of erythroid lineages and thereby leading to thrombocytosis and tumor-associated hypercoagulability (64). Here, AHR is linked to neoplasm.