These data from iPSC-MNs combined with patient fibroblasts data suggest that ALS-linked NEK1 LOF mutations may contribute to disease pathogenesis by affecting primary ciliogenesis, tubulin acetylation, and neuronal survival, and that HDAC6 inhibition has indeed a beneficial effect on the neuronal survival with NEK1 mutations. This evidence concerns the gene HDAC6 and amyotrophic lateral sclerosis.