found that truncated APC mutations in colorectal cancer strongly synergize with MEK inhibitors to enhance WNT responses.[22] When this study was ongoing, a clinical investigation reported the association between RNF43 mutations and anti‐BRAF/EGFR therapies in BRAFV600E colorectal cancer patients, suggesting cross‐talk between the WNT and MAPK pathways and supporting the findings of this study.[23] Our results demonstrate that B‐RAF is a direct ubiquitination target of RNF43, adding a new level of interplay between these two signaling pathways. Here, BRAF is linked to colorectal cancer.