The cardiac late sodium current (INa,L) has been in the focus of research in the last decade. The first reports on the sustained component of voltage activated sodium current dates back to the early seventies, but early observations interpreted this tiny current as a product of a few channels that fail to inactivate having neither physiologic nor pathologic implications. INa,L has emerged recently as a potentially major arrhythmogenic mechanism in various heart diseases attracting the attention of both clinicians and researchers. Research activity on INa,L has exponentially increased since Ranolazine, an FDA-approved antianginal drug was shown to successfully suppress cardiac arrhythmias by inhibiting INa,L. This review aims to conclude a series of papers concerned with physiology and regulation of cardiac late sodium current. Focusing on some recent development of the field we discuss here critical evidences implicating INa,L as a potential target for treating myocardial dysfunction and cardiac arrhythmias.