There is substantial evidence of their essentiality for neuronal function and viability, as is well‐illustrated in those neurological disorders characterized by the absence of one or more ganglioside groupings, for example, absence of the ganglio‐series gangliosides in early‐onset hereditary spastic paraplegia due to disruption of the B4GALNT1 (GM2/GD2 synthase) gene with loss of the ganglio‐series gangliosides (principally GM1, GD1a, GD1b, GT1b as well as the c‐series) [3]. Here, B4GALNT1 is linked to hereditary spastic paraplegia.