Zhu et al. [66] have shown that the iminosugar D-lentiginosine, whose structure is closely similar to that of calystegine B2, stimulated autophagy effectively by upregulating Beclin 1, thus causing the conversion of LC3-I to LC3-II through an inhibition of Akt/mTOR signaling by downregulating the expression of Akt and repressing its phosphorylation; these observations could thus correlate with the fact that calystegines have not exerted any upregulation effect on the Akt gene expression, already repressed under the metabolic syndrome condition. The gene discussed is MTOR; the disease is metabolic syndrome.