Copy number variation may, therefore, make a significant contribution to phenotypic variation in aneuploidy and other chromosomal abnormalities. Targeted analysis of such variation might, therefore, represent an effective strategy for refining critical regions and pinpointing genes central to key pathways (i.e. of cardiogenesis or oncogenesis). This would also help to enable the prediction of which individuals may develop serious phenotypes, such as CHD in DS, which may add an extra dimension to antenatal screening programmes in the future by contributing to the process of 'informed choice' by the potential parents of a DS child, as well as well as aiding the long term management of these patients. Additional benefits may also accrue from increased understanding of pathogenic mechanisms relevant to patients with similar phenotypes outside the context of chromosomal imbalance. In summary, recent technological advances, such as high-resolution array CGH and second-generation sequencing, have vastly and rapidly increased our knowledge of copy number variation in the human genome. As these techniques continue to improve, and greater numbers of samples and populations are investigated, so our understanding of how copy number correlates with phenotype will grow, yielding information not just relevant to individuals with chromosomal imbalances, but to similar conditions in the wider population. Hepatitis Associated Aplastic Anemia: A review Hepatitis-associated aplastic anemia (HAAA) is an uncommon but distinct variant of aplastic anemia in which pancytopenia appears two to three months after an acute attack of hepatitis. HAAA occurs most frequently in young male children and is lethal if leave untreated. The etiology of this syndrome is proposed to be attributed to various hepatitis and non hepatitis viruses. Several hepatitis viruses such as HAV, HBV, HCV, HDV, HEV and HGV have been associated with this set of symptoms. Viruses other than the hepatitis viruses such as parvovirus B19, Cytomegalovirus, Epstein bar virus, Transfusion Transmitted virus (TTV) and non-A-E hepatitis virus (unknown viruses) has also been documented to develop the syndrome. Considerable evidences including the clinical features, severe imbalance of the T cell immune system and effective response to immunosuppressive therapy strongly present HAAA as an immune mediated mechanism. However, no association of HAAA has been found with blood transfusions, drugs and toxins. Besides hepatitis and non hepatitis viruses and immunopathogenesis phenomenon as causative agents of the disorder, telomerase mutation, a genetic factor has also been predisposed for the development of aplastic anemia. Diagnosis includes clinical manifestations, blood profiling, viral serological markers testing, immune functioning and bone marrow hypocellularity examination. Patients presenting the features of HAAA have been mostly treated with bone marrow or hematopoietic cell transplantation from HLA matched donor, and if not available then by immunosuppressive therapy. New therapeutic approaches involve the administration of steroids especially the glucocorticoids to augment the immunosuppressive therapy response. Pancytopenia following an episode of acute hepatitis response better to hematopoietic cell transplantation than immunosuppressive therapy. Aplastic anemia, acquire or congenital anemia associated with hypoplastic "fatty or empty" bone marrow and global dyshematopoiesis, has been first described by Paul Ehrlich in year 1888 [1] . The pathophysiology is believed to be idiopathic [2] or immune-mediated phenomenon with active destruction of haematopoietic stem cells [3] . The abnormal immune response may be elicited by environmental exposures, such as to chemicals, drugs, viral infections and endogenous antigens generated by genetically altered bone marrow cells [4] . A small fraction of the genes involved in pancytopenia has been represented by the congenital BM failure syndromes (relatively rare) which lately develop in clinical syndromes as Fanconi's anemia, Dyskeratosis Congenita, and Shwachman-Diamond syndrome [5, 6] .