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This study provides the first experimental evidence that a single nucleotide mutation within the coding region of the β-globin gene affects mRNA expression levels and causes a β-thalassemic defect. Furthermore, our data suggest that other regions besides the 3′UTR, whose role in constitutively regulation of this mechanism has been recently identified, may contribute to the stabilization of β-globin mRNA and could, therefore, help to characterize the molecular basis of thalassemic hemoglobinopathies

Defective mRNA levels are responsible for a -thalassemia phenotype associated with Hb Federico II, a novel hemoglobin variant [ -106 (G8) Leu->Val]