Among other novel points of interest, the IPA revealed central roles of i) huntingtin cross-talk with nuclear factors modulated by Ranbp2, a mechanism which is thought to be disrupted in Huntington's disease (HD) [84], and ii) two secreted and extracellular signaling proteins, wingless-type MMTV integration site family, member 2 (WNT2B) and brain-derived neurotrophic factor (BDNF), intersecting multiple nodes modulated by Ranbp2 and other factors. This evidence concerns the gene WNT2B and juvenile Huntington disease.