Taken together, these results suggest that (1) individual AKT isoforms are redundant in promoting KPC in vitro growth; (2) AKT1 was sufficient for sustaining fast KPC growth, consistent with the growth-promoting role of this isoform in most non-cancer cell types [8]; (3) whereas AKT3 (and supported by AKT2) contributed more to the phosphorylation of the downstream effectors, PRAS40 and GSK3β, they were largely dispensable for KPC cell growth in the presence of AKT1. Here, GSK3B is linked to cancer.