The mechanism by which the mouse model developed HF and AF was due to transgenic overexpression of mammalian sterile 20-like kinase 1 (Mst1; a kinase activated by clinically important pathologic insults such as ischemia/reperfusion which leads to activation of caspases, apoptosis, and dilated cardiomyopathy [23]) together with a decrease in the cardioprotective kinase, phosphoinositide 3-kinase (PI3K; due to expression of a dominant negative PI3K (dnPI3K) mutant [24]). This evidence concerns the gene MST1 and atrial fibrillation.