JUN and intestinal cancer: Phosphorylated c‐JUN forms a ternary complex with TCF7L2 and β‐catenin, and genetic abrogation of c‐JUN in the ApcMin mouse model of intestinal cancer (in which tumors are essentially caused by an aberrantly activated Wnt pathway upon partial loss‐of‐function of Apc; Jackstadt & Sansom, 2016) caused reduced neoplastic size and prolonged life span, suggesting that c‐JUN protein has a central role in β‐catenin‐dependent intestinal tumorigenesis (Nateri et al., 2005).