Embryonic Hbs include:
Hb Gower-1, composed of two ζ globins (zeta globins) and two ε globins (epsilon globins) (ζ2ε2)
Hb Gower-2, composed of two alpha globins and two epsilon globins (α2ε2)
Hb Portland, composed of two zeta globins and two gamma globins (ζ2γ2)
Fetal Hb (Hb F) is produced from approximately eight weeks of gestation through birth and constitutes approximately 80 percent of Hb in the full-term neonate. It declines during the first few months of life and, in the normal state, constitutes <1 percent of total Hb by early childhood. Hb F is composed of two alpha globins and two gamma globins (α2γ2). Adult Hb (Hb A) is the predominant Hb in children by six months of age and onward; it constitutes 96-97% of total Hb in individuals without a hemoglobinopathy. It is composed of two alpha globins and two beta globins (α2β2). Hb A2 is a minor adult Hb that normally accounts for approximately 2.5-3.5% of total Hb from six months of age onward. It is composed of two alpha globins and two delta globins (α2δ2). Classification of hemoglobinopathies
A)  Qualitative
Structural abnormalities
Hb variants: Hb structural variants are qualitative defects that cause a change in the structure (primary, secondary, tertiary, and/or quaternary) of the Hb molecule. The majority of Hb variants do not cause disease and are most commonly discovered either incidentally or through newborn screening. A subset of Hb variants can cause severe disease when inherited in the homozygous or compound heterozygous state in combination with another structural variant or a thalassemia mutation.
Myhre syndrome is a rare genetic disorder inherited in an autosomal dominant fashion. It is caused by mutation in SMAD4 gene. Signs and symptoms
The clinical presentation is variable but includes
developmental and growth delay
athletic muscular built
skeletal anomalies
joint stiffness
characteristic facial appearance
deafness
variable cognitive deficits
tracheal stenosis
aortic stenosis
pyloric stenosisThe facial abnormalities include:

blepharophimosis (an abnormally narrow gap between the upper and lower eyelids)
maxillary hypoplasia (underdevelopment of the upper jaw)
prognathism (prominent lower jaw)The skeletal abnormalities include:

short stature
square body shape
broad ribs
iliac hypoplasia
brachydactyly
flattened vertebrae
thickened calvariaCongenital heart disease and undescended testes have also been reported in association with this syndrome. Genetics
Myhre syndrome is due to mutations in the SMAD4 gene. This gene encodes a protein - transducer mediating transforming growth factor beta. Some researchers believe that the SMAD4 gene mutations that cause Myhre syndrome impair the ability of the SMAD4 protein to attach (bind) properly with the other proteins involved in the signaling pathway. Other studies have suggested that these mutations result in an abnormally stable SMAD4 protein that remains active in the cell longer. Changes in SMAD4 binding or availability may result in abnormal signaling in many cell types, which affects development of several body systems and leads to the signs and symptoms of Myhre syndrome.The patients of this disease exhibit hypertrophic phenotype in their muscle tissues. Myostatin target genes are found to be downregulated while bone morphogenetic protein (BMP) target genes display both upregulated and downregulated genotypes. Diagnosis
Treatment
History
This disorder was first reported in 1981. It has many similarities to LAPS Syndrome and they both arise from the same mutations in the SMAD4 gene.