Investigating the effect of CB1R activation either by the synthetic cannabinoid arachidonyl-2′-chloroethylamide (ACEA) or by hyperglycemia in hRPTCs revealed that both conditions increased pAKT and pS6 in a PI3K-dependent manner, since their effects were completely prevented by the PI3K inhibitor wortmannin and partially by the CB1R inverse agonist JD5037 (Fig. 3a–f). Here, CNR1 is linked to Hyperglycemia.