Patients affected by the inherited neurodegenerative disease spinal muscular atrophy (SMA) have low levels of survival motor neuron (SMN) protein. SMN has numerous cellular roles, such as the assembly and maturation of small ribonucleoproteins (snRNPs), and the trafficking of mRNAs in neuronal cells. During snRNP maturation, SMN interacts with Sm family proteins, including small nuclear ribonucleoprotein-associated protein (SNRPB) and the neural-specific small nuclear ribonucleoprotein-associated protein (SNRPN). Now, Judith Sleeman and colleagues (Thompson et al., 2018) determine the human neuronal cell line interactomes of SNRPB and SNRPN and find that the essential neural protein neurochondrin (NCDN) interacts with these Sm proteins and SMN. The interactions likely take place within small cytoplasmic vesicles, which the authors have previously shown to be enriched in SMN and Sm family proteins. Interestingly, NCDN and SMN are mutually dependent for their correct subcellular localisation to vesicles, where they colocalise in the context of the early endosome and endocytic marker Rab5. The identification of a novel interaction between NCDN and SMN may shed light on the cause of SMA pathologies, placing NCDN as a potential therapeutic target for SMA treatment.