How PLA2G6 mutations induce the aggregation of α-synuclein is not clear, but as infantile neuroaxonal dystrophy is primarily characterised as an iron storage disorder, and iron dyshomeostasis has been implicated in α-synuclein aggregation (Xiao et al. 2018), one could speculate that elevated iron levels could be associated with α-synuclein aggregation in infantile neuroaxonal dystrophy. This evidence concerns the gene SNCA and neurodegeneration with brain iron accumulation 2A.