In pancreatic cancer, LB-1 decreased the activity of HIF-1α via inhibiting its upstream pathway PI3K/Akt/mTOR, moreover, LB-1 could inhibit the connection between HIF-1α, p-STAT3 and p300, repressing VEGF expression, in addition, LB-1 accelerated HIF-1α degradation by ubiquitin–proteasome pathway [98]. Here, AKT1 is linked to pancreatic neoplasm.