**1. Introduction**

β-Thalassemia syndromes are a group of hereditary blood disorders characterized by reduced or absent β-globin chain synthesis, resulting in reduced Hb in red blood cells (RBCs), decreased RBC production, and anemia. β-Thalassemia includes three main forms: Thalassemia Major, variably referred to as "Cooley's Anemia" and "Mediterranean Anemia," Thalassemia Intermedia, and Thalassemia Minor also called "β-thalassemia carrier," " βthalassemia trait," or "heterozygous β-thalassemia" [1].

The β-thalassemia syndromes are much more diverse than the α-thalassemia syndromes due to the diversity of the mutations that produce the defects in the β-globin gene. The severity of β-thalassemia relates to the degree of imbalance between the α- and non-α-globin chains. The

β-globin gene maps in the short arm of chromosome 11, in a region that contains also the delta globin gene, the embryonic epsilon gene, the fetal gamma genes, and a pseudogene (ψB1) [1].

Unlike the deletions that constitute most of the α-thalassemia syndromes, β-thalassemias are caused by hundreds of mutations that affect all aspects of β-globin production: transcription, translation, and the stability of the β-globin product [2].
