The assumption that GLA p.(Arg118Cys) is a pathogenic variation causing a later‐onset FD phenotype was based on theoretical considerations about the similarities of the structural changes it induces in the α‐Gal monomer and of its in vitro overexpression levels, with those of well‐known missense GLA variations associated with later‐onset clinical phenotypes, as well as on the reasoning that its sulfhydryl‐binding potential might interfere with the normal disulfide bonds of the α‐Gal monomers (Spada et al., 2006). Here, GLA is linked to Fabry disease.