Then, to determine whether interaction between SOD1-G93A and AP2 compete with the interaction between P2X4 and AP2, we conducted pull-down assays from spinal cord protein extracts from WT and SOD1-G93A mice at different time points of the ALS disease (P40, P75, P100 and P120) using, as a bait, an immobilized peptide corresponding to the C-terminal domain of mP2X4 (CT-X4) [52]. This evidence concerns the gene P2RX4 and amyotrophic lateral sclerosis.