We can even speculate that deficits in membrane-bound KCC2 alone—either through T1007 phosphorylation-dependent reduced membrane KCC2 abundance in preBötC neurons and/or impaired Rab11b-mediated KCC2 trafficking, or in conjunction with other synaptic impairments—could contribute to the respiratory failure associated with the Tgf-β2−/− phenotype [49]. The gene discussed is RAB11B; the disease is respiratory failure.