No δ or β synthesis due to deletion of the coding sequences for both δ- and β-globin. Milder clinical phenotype than β0-thalassemia because the remaining γ gene(s) is still active after birth instead of switching off as would normally occur. Therefore, HbF (α2γ2) compensates for the absence of HbA (αβ), about 5-18% of normal level of total hemoglobin production.