PLN and atrial fibrillation: We suggest that dysfunction of atrial repolarization and abnormality of the intracellular Ca2+ handling protein (L-type calcium channel a1c (LVDCCa1c), calcium adenosine triphosphatase (Ca2+-ATPase), ryanodine receptor type-2 (RYR2), inositol triphosphate receptor type-1(IP3R1) or ancillary proteins phospholamban (PLN) in the microenvironment increase with ageing, and thus create a substrate for initiation and maintenance of AF.