Next, we used statistical colocalisation29 to identify loci where the same causal variant appeared to be driving both an iPSC eQTL and an association with one of 14 complex traits, identifying 233 loci where the posterior probability of a joint association exceeded 0.5 (Supplementary Table 6). Of these, 45 were iPSC-specific, including PTPN2, an iPSC-specific eQTL that strongly colocalised with risk variants for four autoimmune disorders (Fig. 5a). Previous eQTL studies in both immune cells30–32 and GTEx tissues have not identified a PTPN2 eQTL (Extended Data Fig. 9), suggesting that disease risk variants at PTPN2 may function in stem cells, or early development.
