This profile entails the stimulation of cell cycle genes.19 Human ischaemic and non‐ischaemic heart failure activates the Hippo pathway, while its inactivation reverses systolic heart failure after MI.20 Another YAP‐related activity is the modulation of antioxidant capacity, where YAP inactivation suppresses FoxO1 activity and decreases antioxidant gene expression, thus aggravating ischaemia‐reperfusion induced heart injury.21 Here, YAP1 is linked to systolic heart failure.