The most common of these are the regulatorychanges (including whole gene deletion) causing α-thalassemia andβ-thalassemia and the following point mutations causingstructural change in the hemoglobin protein: HbS, HbC (which, like HbS, involvesa point mutation in codon 6 of β-globin, this time causing a Glu→Lys change) and HbE (codon 26 of β-globin, Glu→Lys) [231]. Here, HBE1 is linked to thalassemia.