Whilst a potential contribution of specific genetic mutations to slope estimates across the phenotypes could not be discounted, given that point mutations (SOD‐1, FUS or TARDBP) represent ~2% of the Australian ALS cohort and C9orf72 hexanucleotide expansion ~10% [4], it is unlikely that inadvertent inclusion of the genetic cohorts would have appreciably impacted the present findings. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.