FAS and autoimmune lymphoproliferative syndrome: For example, a primate-specific intronic Alu promotes RNA editing of a nearby exon coding for a GABA receptor and consequently lowers the excitability of the neuron [20]; another intronic Alu insertion in the Fas gene causes loss of the next exon in Fas mRNA, without affecting the splice junction, and results in autoimmune lymphoproliferative syndrome [21].