Our study deciphers a protein interaction network through a phosphorylation cascade between MTOR and WNK1/SPAK-OSR1 leading to deregulation of chloride cotransporters, increased neuronal Cl− levels and GABAA dysfunction in malformations of cortical development, linking genomic defects and functional effects and paving the way to target epilepsy therapy. The gene discussed is MTOR; the disease is epilepsy.