GAL and neuroblastoma: Turning to Gal-1 and our cell model, sensing an upregulation of a counter-receptor as the molecular on-switch for a cellular activity, as is the case for homodimeric Gal-1 and the originally cryptic ganglioside GM1 (obtained by tightly controlled removal of one sialic acid from the ganglioside GD1a glycan) in controlling neuroblastoma proliferation (Kopitz et al. 1998, 2001), in autoimmune regulation (Wang et al. 2009) and in neuritogenesis (Wu et al. 2016), would be lost if Gal-1 were not a homodimer but had a tetrameric CRD presentation.