CDKN1B and triple-negative breast carcinoma: In accordance with this, the modulation of nuclear B2 receptors with cell-permeable antagonists (for this type of receptor) proved their involvement in human triple-negative breast cancer via a mechanism involving p38 mitogen-activated protein kinase (p38 kinase)—cyclin-dependent kinase inhibitor 1B (p27kip1) leading to apoptosis and reducing cell proliferation [80].