[8] Proteins in the DHBS family include mammalian SFPQ (splicing factor, proline- and glutamine-rich; a.k.a.

[24] Studies in humans and mice have identified that NONO null mutations likely lead to the development of a clinically recognizable intellectual disability with cognitive and affective deficits.

[25] It was later found that these pathogenic variants were also strongly associated with cardiomyopathy with left ventricular noncompaction and sometimes Ebstein's anomaly.

[29] It is speculated that it is the phosphorylation state on NONO that acts to direct the proteins many disparate functions within the nucleus.

[30] NONO has also been observed within the brain, localised in the cytoplasm of hippocampal neurons that are associated with RNA transport granules.