As PI3K/AKT signaling is involved in a multitude of processes in the progression of cancer, and our results indicate that the loss of E-cadherin is only advantageous to cancer progression at some points of the metastatic pathway, the observed sensitivity of E-cadherin expression to a high threshold of activated AKT expression may represent a means of fine tuning the negative regulation of E-cadherin by PI3K/AKT signaling. Here, AKT1 is linked to cancer.