To test the role of Akt and ERK1/2 hyper activation in AV’s effect on cancer cells, we utilized inhibitors of Akt and ERK1/2 upstream activators, namely, a MEK1/2 inhibitor, Selumetinib (MEK1/2 is ERK1/2 direct upstream activator), a PI3K inhibitor, ZSTK474 (PI3K is an upstream activator of Akt), and IGF1R inhibitor AEW-541 (IGF1R activates both Akt and ERK1/2 pathways). This evidence concerns the gene IGF1R and cancer.