Although slowed contraction has been reported in the SOD1 G93A transgenic murine model, this is the first human-based work to directly demonstrate defective contractile function of ALS muscle in a human-based system37, although a previous researcher did extrapolate functional defects by measuring the passive electrical properties of ALS skeletal muscle generated from patient iPSCs38. Here, SOD1 is linked to amyotrophic lateral sclerosis.