Moreover, although both inactivation (heterozygous deletion of YAP) and activation (homozygous deletion of WW45) of YAP promote heart failure in response to pressure overload, combined deletion of YAP (heterozygous) and WW45 (homozygous) in cardiac myocytes is protective against pressure overload–induced cardiac dysfunction (Ikeda et al. 2019). The gene discussed is SAV1; the disease is heart failure.