Moreover, genetic deletion of the MNK1/2 kinases, which phosphorylate eIF4E, administration of the MNK1/2 inhibitor cercosporamide, or substitution of the eIF4E phosphorylation site for a non-phosphorylatable residue (Eif4eki/ki mice; Ser209Ala), ameliorated FXS phenotypes in Fmr1-/y mice (Gkogkas et al., 2014). The gene discussed is FMR1; the disease is fragile X syndrome.