Interestingly, this study strongly advocates the existence of a crosstalk between mutated FBXW7 and several other proteins in ATL cell lines, such as viral oncogene (HTLV‐I Tax), p53, c‐Myc, etc. Given the high rate of mutation in both p53 and c‐Myc in human carcinomas, selective loss of FBXW7 functions may play a more decisive role in the oncogenic process. Here, FBXW7 is linked to carcinoma.