For angiogenesis-enriched signature pairs, we observed highly exposed genes in both scz and t2d signatures, e.g. IL18, APLNR, NGFR, TYMP, SPRED1 and HPSE. Some of these genes including IL18, APLNR, NGFR and SPRED1 were already shown to be dysregulated in various processes such as inflammation, energy metabolism, peripheral neuropathy and cell plasticity in both diseases [34–42]. Here, APLNR is linked to peripheral neuropathy.