This result is in line with the “cAMP theory of Fragile X Syndrome”, which is based on several observations: cAMP production is reduced in the blood platelets of Fragile X patients [76,77], in the brain of drosophila and mouse Fragile X models and in neural precursor cells from human Fragile X fetal tissues [78]; phosphodiesterase 2a (an enzyme breaking down cAMP) is one of the main targets of physiological FMRP inhibitory control [79], and is thus overactive in Fmr1 KO mouse neurons, leading to reduced cAMP levels [80]. The gene discussed is FMR1; the disease is fragile X syndrome.