Cardiac function (FS) of mice treated with Ccnd1 or Ccnd2 was significantly improved compared to Ttn shRNA mice treated by EGFP. Ccnd1 or Ccnd2 overexpression significantly suppressed DCM induced by Ttn shRNA, suggesting cyclin D serves as a crucial downstream of Yy1 to enhance cardiac performance (Supplementary Table S5). The gene discussed is CCND2; the disease is familial dilated cardiomyopathy.