Model describing the role of G9a established H3K9me2 in regulation of fetal and adult β-globin genes expression in adult erythrocytes. G9a establishes H3K9me2-dependent repressive chromatin protecting the γ-globin gene promoters from interaction with the LDB1 complex and the LCR in adult erythroid cells. Inactivation of G9a methyltransferase activity (MT) causes elimination of H3K9me2 from the γ-globin gene promoters, facilitating LDB1 complex occupancy and interaction with LCR.