**7. Post translational mechanisms**

A few, comparatively uncommon, mutations that cause thalassemia by disrupting the structure of the fully translated globin product. That appears to interfere with normal folding of the globin peptide to form stable dimers or tetramers. In each case, the abnormal globin generates inclusion bodies and produces a thalassemia phenotype. The final common pathway for these mutations is similar to that of the dominant form of thalassemia due to nonsense codons in the final exon. In all circumstances, accumulation and generation of substantial amounts of the abnormal protein results in formation of inclusion bodies [34, 35, 38].
