GSTM1 and subarachnoid hemorrhage: An interesting implication of NO in the pathogenesis of delayed cerebral ischemia following subarachnoid hemorrhage (SAH) has been proposed, suggesting both eNOS and nNOS dysfunctions are among the mechanisms of the disease [114]. Driven by immunological and nonimmunological processes, red blood cells (RBCs) of the subarachnoid clot hemolyze resulting in delayed occurrence of cell-free Hb in the cerebrospinal fluid.