Storage lesion of red blood cells (RBCs) is a well-recognizedprocess characterized by complex morphological and functional changes. Those changes deteriorate the life-saving quality of stored blood with a reported increase in mortality for some categories of patients receiving “old” versus “new” blood. The importance of RBC cation gradients (K+and Na+) dissipation in the process of storage lesion has been recently highlighted. Here we report a previously unrecognized nonselective cation channel in human RBCs (patch-clamp) activated whenever extracellular Ca2+ is removed and very likely contributing to the cation gradients dissipation when opened. In view of the existence of such a channel the use of non-Ca2+-chelating anticoagulants like heparin, preventing channel opening, can reduce cation gradients dissipation and help limit and delay RBCs storage lesion.