Subsequent research has further explored how dysregulation of the Hippo signaling pathway, such as the deletion of scaffold protein Sav1 (also known as Salv1; Salvador homolog 1) or the downstream effectors Lats1 and Lats2, as well as the overexpression of YAP in adult cardiomyocytes, can stimulate cardiomyocyte proliferation and improve heart regeneration following MI injury [109–111]. The gene discussed is SAV1; the disease is myocardial infarction.