Recent advances in molecular biology has resulted in the characterization of different forms ofα-thalassemia (α-thal). Deletion, or occasionally dysfunction, of one or bothαglobin genes, which are located on the short arm of chromosome #16 (l), will lead to anαchain deficiency with variable alterations in red cell indices.α-Thal-2 orαα/-αresults from deletion of one of the two a globin genes, i.e. either the leftward or 4.2 kb deletion involving theα2globin gene or the rightward or 3.7 kb deletion which involves the 3′segment of theα2gene, the 5′segment of the a1 gene and intergenic DNA.α-Thal-1 orαα/- results from larger deletions involving segments of DNA which contain both theα2 globin gene and (part of) theα1 globin gene. The various types are due to misalignment between two strands of DNA from two separate chromosomes during meiosis followed by an unequal crossover generating chromosomes with a single (or no) functional a globin gene or with triplicated a globin genes (2, and references quoted). Appropriate combinations of these chromosomes will lead to anα-thal-2 homozygosity (α-/α-), to Hb H disease (−/α-), to hydrops fetalis (- - / - -), and to genetic conditions such as those characterized by the presence of five (ααα/αα), four (ααα/α-) or three (ααα/−) a globin genes (2,3,4)