We and others have previously shown that IL11 signaling, and to a lesser extent IL6 trans‐signaling, enables and promotes the formation and progression of epithelial tumors that arise in the intestinal epithelium in response to aberrant canonical WNT signaling associated with either loss‐of‐function mutations in the Apc tumor suppressor gene or gain‐of‐function mutations in β‐catenin (Becker et al, 2004; Ernst et al, 2008; Putoczki et al, 2013). The gene discussed is IL6; the disease is neoplasm.