Atrial fibrillation (AF) is a serious condition in which there is abnormal rhythm in the atria of the heart. This increases the risk of stroke, with AF patients having a high mortality rate and reduced quality of life. Unfortunately, many AF patients show limited improvement with current treatment options. We therefore aim to investigate a new target for treating AF. One of the underlying causes of AF is altered calcium handling in the heart. In particular, the calcium channel known as the ryanodine receptor (RyR2) has abnormal activity in AF patients; however, the mechanisms causing this change remain under-studied. We will investigate how RyR2 activity is modified by an associated protein – calsequestrin (CSQ2) and use CSQ2 to normalise RyR2 function and rhythm in atrial samples from AF patients. This will identify a new therapeutic target for treating abnormal calcium handling that occurs in AF to improve symptoms in patients.