For example, we have already noticed in a previous work [41] that miR 129-5p was a known inhibitor of the biosynthesis of gamma-globin 2, a subunit of human fetal hemoglobin, replaced in adults by beta-globin, also dysregulated in some blood diseases, like the other subunit alpha-globin, by several miRs, including miR 451a [42,43,44,45,46]. The gene discussed is HBG2; the disease is blood disease.