The study examined 18 European patients with heterozygous variants in the KIF1A gene, which is responsible for the disorders known as KAND (KIF1A-associated neurological disorder). Most of the variants were located in the motor domain of the protein and the clinical symptoms varied from the very severe congenital phenotype to mild forms of spastic paraparesis or slowly progressive neuropathy. In 13 patients with early onset of symptoms (congenital symptom, motor developmental delay, or spastic paraplegia), all missense variants were detected in the motor domain, eight times being confirmed as de novo mutations. Five adult-onset patients had spastic paraplegia, with one having a frame shift variant outside the motor domain. The study concluded that KAND phenotypes are not limited to severe early-onset forms, but also include less severe adult-onset forms. Localization of a missense variant in the motor domain of KIF1A correlates with more severe disease, but it is not the exclusive rule. The authors propose an algorithm to individually evaluate each variant in terms of its pathogenicity and prediction of the associated phenotype.