AKT1 and colorectal carcinoma: In these cells, Akt was either over-expressed by transfection with a constitutively active Myr-Akt1 plasmid, or AMPK activity was inhibited by compound C. As shown in Figure 2A, both over-expression of Akt and suppression of AMPK activity rescued cell proliferation inhibited by CAPE or CAPPE treatments in human CRC HCT-116 cells.