The cross‐sectional analysis in this study concurs with these findings, showing levels of CHIT1, CHI3L1 and CHI3L2 concentrations, as well as CHIT1 activity, to be similar in healthy controls and at‐risk individuals who have not yet phenoconverted (irrespective of genotype), but elevated in symptomatic ALS compared to both healthy controls and at‐risk individuals. Here, CHI3L1 is linked to amyotrophic lateral sclerosis.