The pathogenesis of ventricular tachycardia (VT) in most patients with a prior myocardial scarring is reentry involving compartmentalized muscle fibers protected within the scar. Often the 12-lead ECG morphology of the VT itself is not available when treated with a defibrillator. Consequently, VT ablation takes on an interesting challenge of finding critical targets in sinus rhythm. High-density recordings are essential to evaluate a substrate based on whole electrogram voltage and activation delay, supplemented with substrate perturbation through alternate site pacing or introducing an extra stimulation. In this article, we discuss contemporary intracardiac electrogram targets for VT ablation, with explanation on each of their specific fundamental physiology.