Paroxysmal nocturnal hemoglobinuria (PNH) is embedded with idiopathic/immune aplastic anemia (AA) because of both common pathophysiology and clinical association. Indeed, over 40% of AA patients may exhibit a PNH population within their mature blood cells, and the expansion of hematopoietic progenitors carrying the PIGA mutation (the somatic mutation eventually accounting for PNH) is not considered a random phenomenon in AA since PIGA-mutated cells are thought likely to be able to escape from the (auto)immune attack causing AA (Ref Neal/jarek and Luzzatto/rotoli, plus notaro/gargiulo). Clinically speaking, the spectrum of overlap between PNH (which is clinically characterized by the triad of hemolysis, thrombophilia, and bone marrow failure (BMF)) and AA ranges from classical PNH with nonmeaningful cytopenia to typical AA with nonmeaningful PNH clonal populations (i.e., subclinical PNH). Meaningful clinical overlap between PNH and AA is described as AA/PNH syndrome or intermediate PNH, depending on the severity of cytopenia. Here, we will focus on the diagnosis and management of bone marrow failure associated with PNH, highlighting that the management of these patients is not different from that of patients with isolated AA (i.e., in the absence of meaningful PNH clonal populations). Except for the higher risk of thrombosis, patients with AA and a PNH clone should be managed the same way as compared to patients with idiopathic anemia without a clone. Sibling transplantation is mandatory for patients aged less than 40–50 when a matched family donor is available; immunosuppression using the association of horse antithymocyte globulin (ATG), cyclosporine, and eltrombopag (paying attention to the increased risk of thromboembolic complications) is the reference treatment for other patients. In some very rare cases, a significant intravascular hemolysis is associated, which may justify associating a treatment with complement inhibitors. Considering the recent advances in the field of anticomplement therapies, we will also briefly describe the novel data with new complement inhibitors, introducing the concept of proximal inhibitors as well as describing their possible role in changing the treatment paradigm of hemolytic PNH.