A very recent study shows that a drosophila model of Fragile X Syndrome displayed an abnormally increased number of mitochondria and oxidative hyperactivity in the neurons of the neuromuscular junction, together with a reduced locomotor activity; these malfunctions were corrected by treatment with eltoprazine, a selective 5-HT1A receptor agonist [67]. Here, HTR1A is linked to fragile X syndrome.