It is worth noting that also genetic factors unlinked to the beta globin cluster, favour the Hb F synthesis in the post-fetal life [4]. Particularly interesting for its frequency is the polimorphic single-base substitution C→T at Ggamma -158, recognizable for the creation of a XmnI restriction site, that appears to cause an increase of Hb F expecially during erythropoietic stress.