Previous studies have suggested that harmine induces cell cycle arrest or apoptosis through (i) intercalation into DNA and inhibition of protein synthesis [30], (ii) inhibition of DNA repair via homologous recombination [21], (iii) down-regulation of the cyclooxygenase-2 protein abundance in gastric cancer [31], (iv) inhibition of the Akt and ERK signaling pathways [19], or (v) inhibition of dual-specificity tyrosine-phosphorylation-regulated kinase 1A [32, 33]. The gene discussed is AKT1; the disease is gastric cancer.