PRRT2 and cyclic hematopoiesis: These stimuli, which include angiotensin-II, TNF-α and endothelin-1 (ET-1), could mediate CH by interrupting multiple downstream signaling processes (mitogen-activated protein kinases (MAPKs), calcineurin, NF-κB, protein kinase C (PKC) and tyrosine kinases) [106].