Cardiac myocytes derived from human induced pluripotent stem cells (hiPSC-CMs) are a useful and renewable human myocyte model. Despite their promise, these cells have unexplored limitations when applied to action potential (AP) analysis. APs occur spontaneously and are associated with variability due to a small/missing inwardly rectifying potassium channel (IK1). We used whole cell voltage clamp with dynamic clamp to express IK1, which significantly improved the physiological behavior of the AP and electrical profile of hiPSC-CMs.hiPSC-CMs have a negligible peak IK1 at −120 mV (−0.81 ± 0.4 pA/pF) which results in depolarized resting membrane potentials (RMP) (−60.0 ± 1.7 mV, n=17). “Electronic transfection” of IK1 into hiPSC-CMs results in reestablishing a physiological RMP (−84.0 ± 0.2 mV), increases the maximal upstroke velocity (from 82.1 ± 2.4 to 161.6 ± 11.5 mV/ms), reduces AP duration, and increases the rate of repolarization (from 0.35 ± 0.03 to 1.1 ± 0.1 mV/ms, n=17). Despite a detectable transient outward potassium current in hiPSC-CMs, “spike and dome” morphology is generally absent in spontaneously active cells; addition of electronic IK1 restored this morphology in 12 out of 17 ventricular cells. It also restored the relationship between maximum upstroke velocity and sodium current density. The stabilized membrane potential allowed systematic measurement of dynamic parameters. The rate dependence of the AP duration was measured in at different pacing rates from 4000 to 500 ms in 12 electronic IK1 expressing hiPSC-CMs and showed a classical monotonic restitution curve, with AP increasing with increased cycle length. By removing sodium channel inactivation, electronic expression of IK1 improves hiPSC-CMs utility in assess mechanisms involving sodium channels and phase 1 repolarization such as LQT3 and Brugada Syndrome.