Since PI3K/AKT pathway activation is a driving force for cell proliferation and prostate cancer progression in Pb-Cre+;PtenL/L prostate cancer [17], [20], we then examined whether there is any alteration of AKT activation after genetic deletion of CD166. Western blot analysis demonstrated that Pb-Cre+;PtenL/L;CD166−/− prostate has no CD166 expression, but has similar P-AKT levels compared to Pb-Cre+;PtenL/L;CD166+/+ and Pb-Cre+;PtenL/L;CD166+/− prostate (Figure 6D). This evidence concerns the gene AKT1 and Familial prostate cancer.