Beta-thalassemia
Beta thalassemias are due to mutations in the HBB gene on chromosome 11, also inherited in an autosomal, recessive fashion. The severity of the disease depends on the nature of the mutation and on the presence of mutations in one or both alleles. Mutated alleles are called β+ when partial function is conserved (either the protein has a reduced function, or it functions normally but is produced in reduced quantity) or βo, when no functioning protein is produced. The situation of both alleles determines the clinical picture:

β thalassemia major (Mediterranean anemia or Cooley anemia) is caused by a βo/βo genotype. No functional β chains are produced, and thus no hemoglobin A can be assembled. This is the most severe form of β-thalassemia;
β thalassemia intermedia is caused by a β+/βo or β+/β+ genotype. In this form, some hemoglobin A is produced;
β thalassemia minor is caused by a β/βo or β/β+ genotype. Only one of the two β globin alleles contains a mutation, so β chain production is not terribly compromised and patients may be relatively asymptomatic.Beta thalassemia most often occurs in people of Mediterranean origin. To a lesser extent, Chinese, other Asians, and African Americans can be affected. Delta-thalassemia
As well as alpha and beta chains present in hemoglobin, about 3% of adult hemoglobin is made of alpha and delta chains. Just as with beta thalassemia, mutations that affect the ability of this gene to produce delta chains can occur. Combination hemoglobinopathies
Thalassemia can coexist with other hemoglobinopathies.
In 2009, a group of doctors and specialists in Chennai and Coimbatore registered the successful treatment of thalassemia in a child using an unaffected siblings umbilical cord blood. Research
Gene therapy
Gene therapy is being studied for thalassemia. The procedure involves collecting hematopoietic stem cells (HSCs) from the affected persons blood. The HSCs then have a beta-globin gene added using a lentiviral vector. After destroying the affected persons bone marrow with a dose of chemotherapy (a myeloablative conditioning regimen), the altered HSCs are infused back into the affected person where they become engrafted in the bone marrow where they proliferate. This potentially results in a progressive increase in hemoglobin A2 synthesis in all subsequent developing red blood cells, with resultant resolution of the anemia.While one person with beta thalassemia has no longer required blood transfusions following treatment within a research trial, it is not an approved treatment as of 2018. HbF induction
HbF induction is an attempt to reactivate fetal globin gene transcription. Efforts involve trying to disrupt the fetal globin gene promoter. References
External links

Thalassemia at Curlie
Learning About Thalassemia published by the National Human Genome Research Institute.