There was a significant excess of splice-disrupting variants in PKP2 in people with ACM (excess burden in cases = 5.9%, P < 0.001), FLNC (2.7%, P < 0.001) and TTN (2.8%, P < 0.001) in people with DCM, MYBPC3 (8.2%, P < 0.001) and MYH7 (1.3%, P < 0.001) in people with HCM, and KCNQ1 in people with LQTS (3.6%, P < 0.001) (Supplementary Table 2). Here, PKP2 is linked to familial dilated cardiomyopathy.