There is considerable evidence suggesting that the switch from gamma to delta and beta chain production after birth is due, in part, to silencing of the gamma genes by stage-specific factors which bind to their promoters and to the competition from the adult (delta and beta) genes for a common enhancer element located in the locus control region. As a consequence one can expect that the increased Hb F production in adults with hereditary persistence of fetal hemoglobin or delta beta-thalassemia is directed mainly by gamma-globin genes in cis to the deletion(s) responsible for these conditions. Here we review data on heterozygotes with gamma-, delta- or delta beta-thalassemia, who also had an A gamma T mutation, in cis or in trans, which was used as a marker of gamma gene expression. The results show that a deletion affecting adult beta genes favors the expression of gamma genes in cis, while the deletion of a single gamma gene does not affect the expression of the beta gene in cis but leads to a faster gamma-->beta switch postnatally.