Afadin is phosphorylated at serine 1718 by Akt, which is activated in response to insulin-like growth factor-1, or by oncogenic alterations in the phosphatase and tensin homolog–PI3K–Akt pathway, and translocated into the nucleus, disrupting the AJs and enhancing migration in breast cancers (64). This evidence concerns the gene AKT1 and breast carcinoma.