Whereas CB1R may restrain potentially deleterious mTORC1 over-activation during normoglycemia by preventing amino acid flux, in diabetes, enhanced activity of CB1R by eCBs, stimulates mTORC1 to further increase glucose uptake via upregulating SREBP1-mediated GLUT2 expression, thus contributing to the development of DKD (Fig. 8). This evidence concerns the gene SLC2A2 and diabetes mellitus.