An anti-metastatic mechanism, induced upon activation of ACE2/Ang-(1–7)/Mas axis has been recently described in a breast cancer model that includes repression of store-operated calcium entry (SOCE)-induced PAK1/NF-κB/Snail1 signal pathway, ultimately resulting in decreased expression of Snail1 and increased production of E-cadherin [59]. Here, SNAI1 is linked to breast carcinoma.