Results showed that BA induced p53 expression and activation till 12 h in HCT116 and HT29 cells and till 4 h in SW480 cells, and then rapidly degraded p53 in three CRC cells (Figure 6d; Etoposide was used as a positive control to activate p53 in CRC cells (Supplementary Figure S6)), suggesting that short exposure to BA firstly activates p53 and then rapidly degrades p53 by the ubiquitin–proteasome pathway. This evidence concerns the gene TP53 and colorectal carcinoma.