Our detection of a strong collaboration between the integrin‐FAK and BRD4‐MYC axes in the promotion of cell survival is also in line with the crosstalk between the integrin‐FAK axis and the Akt/mTOR or Wnt/β‐catenin pathway in CRC [7, 9, 20, 31], and their links to CRC stemness and disease recurrence [23]. This evidence concerns the gene AKT1 and colorectal carcinoma.