Conversely, upon its P4-mediated activation, mPRα exerts inhibitory effects on cell proliferation and migration in triple-negative breast cancer [145] and in basal phenotype breast cancer via FAK dephosphorylation, MMP9, Vascular-Endothelial Growth Factor (VEGF), and Calcium-Activated Potassium Channel Subunit alpha-1 (KCNMA1, also known as BK channel alpha subunit or large conductance Ca2+-activated potassium channel, subfamily M, alpha member 1, KCa1.1) downregulation mechanisms [146]. Here, VEGFA is linked to breast cancer.