Atrial fibrillation (AF) affects 9% of the aging population and often causes life threatening complications like stroke. AF originates from changes to the cardiac tissue and its electrical impulses leading to ‘quivering’ of the upper chambers of the heart, causing them to be inefficient in pumping and emptying blood. Current treatment options for AF include lifestyle changes, non-specific drugs, and surgery, to help prevent blood clots, or to restore the heart’s normal rhythm, all with their own set of side-effects. An increase in the enzyme Protein kinase C-_ (PKCε) stimulates the activity of the ion channel protein GIRK1/4, which drives the electrical instability of the atria, leading to AF. GIRK1/4 is a K+ channel that is crucial to atrial rhythm. PKCε can be activated by natural increases in H2O2 in the cell through the aging process. We developed an optogenetically activated PKCε enzyme that moves from inside the cell to the cell membrane in response to blue light as well as H2O2. We also show that this light-activated PKCε enhances GIRK1/4 activity. We used human cardiac stem cells that beat spontaneously and studied their behavior in response to a PKCε activator. This explicit and consummate insight is guiding the search for a better, more specific drug aiming to reverse the increase in GIRK1/4 activity responsible for AF.