Given that the SOD1 transgenic mouse is one of the most highly studied and characterized models of ALS, we crossed SOD1G93A mice with IL6R trans-signaling mice to determine how enhanced trans-signaling influences motor weakness and pathological processes, including neuromuscular junction (NMJ) denervation, glial activation and motoneuron (MN) survival. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.