In NSCLC A549 cells, extracts of total ginsenosides upregulated the protein expression of ATF4, CHOP and BIP, inhibited AKT-1 and p70 S6 kinase phosphorylation, increased ATG7 expression levels, activated ERS, promoted LC3-II levels and autophagosome formation, and increased autophagic flux, thereby inducing cell autophagic death, a process that is mediated via the ATF4-CHOP-AKT1-mTOR axis (Zhao et al., 2019). The gene discussed is AKT1; the disease is non-small cell lung carcinoma.