While the observed switch of cytokine dependency from IL-11 to IL-6 during tumor progression is consistent with the recognized role of IL-6 as a master regulation across many cell types within the tumor microenvironment and a broadening of responsive cells through inflammation-associated IL-6 trans-signaling,46 the latter only contributes marginally to the growth of gastric organoid tumors in a subcutaneous setting. Here, IL11 is linked to neoplasm.