Artemisianins A exhibited a strong repressive effect on CRC HT-29 cells with an IC50 value of 7.2 μM, and it increased the expression of IRE1α and XBP1s, upregulated autophosphorylated p-PERK and PERK-mediated p-eIF2α phosphorylation, and upregulated the expression of ATF6 and CHOP, suggesting that artemisinin A triggered apoptosis in HT-29 cells and activated ERS apoptotic signaling for tumor suppression by upregulating the UPR pathway of IRE1α, p-PERK, ATF6 and CHOP and by disrupting intracellular Ca2+ homeostasis (Xue et al., 2019). This evidence concerns the gene DDIT3 and neoplasm.