To further validate these findings, we analyzed a recently published ALS postmortem spinal cord RNA sequencing (RNA-seq) dataset and found reduced expression of ANK3, as well as mis-regulation of other AIS genes, such as KCNQ2 and SCN1A (Figure S1C).30 In addition, we optimized ankyrin-G staining of ventral horn spinal MNs in postmortem tissue (Figure S1D) and found that AIS length was reduced in sporadic ALS and TDP-43-associated ALS cases compared to control cases (Figures S1E–S1G), supporting our in vitro data showing a switch from a longer to a shorter AIS in late ALS hiPSC MNs. The gene discussed is SCN1A; the disease is amyotrophic lateral sclerosis.