Through in vivo transgenic mouse studies, utilising global and inducible cell type-specific deletion of TREK-1, Abraham and colleagues were able to demonstrate that TREK-1 is an important modulator of cardiac hypertrophy, diastolic function and fibrosis in mouse hearts; with differential influence on cardiac dysfunction when TREK-1 is expressed in myocytes compared to fibroblasts [234]. Here, KCNK2 is linked to cardiac hypertrophy.