Transcription factor 4 (TCF4) was a key regulator of ERS, and tumor protein p53 (TP53) could inhibit TCF4 activity; in CRC LoVo and RKO cells, oridonin upregulated the expression of TP53 in a concentration-dependent manner, which inhibited the activity of TCF4 and caused the cellular ROS aggregation and disrupting Ca2+ homeostasis, and elevating the expression levels of ATF4 and CHOP, which ultimately led to apoptosis; this suggested that Oridonin exerts its antitumor effects by regulating ERS induced via the TP53/TCF4 axis (Zhou et al., 2023). The gene discussed is TP53; the disease is colorectal carcinoma.