Our Co‐IP assays demonstrated markedly reduced FBW7 R465C‐MCL1 binding compared to wild‐type FBW7, leading to impaired degradation and consequent upregulation of MCL1 in R465C‐mutated patient‐derived CRC tumor tissues and experimental models, which is consistent with the previous finding [15, 20]. The gene discussed is MCL1; the disease is neoplasm.