In D. melanogaster, FDL-deficient mutants showed paucimannose-deficiency and, notably, caused locomotion defects in fruit flies, indicating that Hex and/or paucimannosidic proteins are involved, via elusive pathways, in essential fruit fly processes. As expected, the less-consequential monoallelic fdl mutation was shown to result in reduced paucimannosidic protein formation and caused a non-lethal, but still severe phenotype, by halting the generation of peripheral long-term memory neurons. Impaired generation of peripheral long-term memory neurons was also observed for fruit fly fdl and MgatI null mutations, which, in turn, resulted in infertility and locomotion defects. The lack of fucosylated paucimannosidic glycans was proposed to contribute to neuronal impairment in both fdl and Mgat1 mutants. The importance of fucosylated paucimannosidic glycans was supported by a study reporting that mutations in the FucT6 gene encoding the D. melanogaster α1,6-fucosyltransferase resulted in an impaired fruit fly immune response towards parasitic infections. Taken together, these phenotypic observations suggest that the fruit fly paucimannosidic glycans, some of which overlap with the human repertoire, are pivotal in the development, immune function and survival processes of D. melanogaster. It was reported that T. castaneum abundantly expresses paucimannosidic proteins during its post-larval stages, recapitulating findings from other studies proposing that paucimannosidic proteins are strongly regulated during early development. Thus, it is likely that paucimannosidic glycans conjugated to still unknown flour beetle carrier proteins, similar to those in nematodes and fruit flies, are vital for growth and survival processes of the flour beetle.