Their result indicated that GGCT silencing downregulated the phosphorylation of PRAS40 (proline-rich AKT substrate of 40 kDa) at Thr246 (Figure 2) and upregulated the cleavage of PARP at Asp214, and that cancer growth control by GGCT occurred, at least in part, through the regulation of apoptosis-related proteins. This evidence concerns the gene AKT1 and cancer.