Table 1. Number of cis-eQTLs driven by the same causal variant as the SLE disease association (total number of SLE loci: 38).

	Gene	Transcript	Exon	Junction	Intron	Total
Causal cis-eQTLsa	2	2	7	4	4	9b
% of 38 SLE GWAS loci	5.3	5.3	18.4	10.5	10.5	23.7
% of total causal eQTLs	22.2	22.2	77.8	44.4	44.4	100
Candidate genes	3	4	9	5	5	12
Expression targetsc	2	7	24	18	13	64

The lead SNPs from the Bentham and Morris et al 2015 GWAS in persons of European descent were functionally annotated by cis-eQTL analysis in the Geuvadis RNA-Seq cohort in lymphoblastoid cell lines using RNA-Seq quantification profiled at five resolutions (gene, transcript, exon, junction, and intron). Only SNPs reaching genome-wide significance, not conditional peaks, outside of the major histocompatibility complex loci, and with minor allele frequency > 5% were included leaving 38 SLE lead SNPs in total. All SLE loci were densely imputed to the 1000 Genomes Phase 3 Imputation Panel as described in methods.

All 38 loci (+/-100kb of each lead SNP) comprised a nominally significant cis-eQTL (P<0.01) for at least one gene within +/-500kb of the lead SNP at each resolution of RNA-Seq. Evidence of a single shared causal variant at each locus was assessed using the Joint Likelihood Mapping (JLIM) algorithm as described in methods.

^aNumber of loci where the disease association is consistent with a single shared effect for at least one cis-eQTL (P<0.01 and JLIM FDR adjusted P<0.05).

^bThe total number of unique causal cis-eQTLs across all RNA-Seq quantification types.

^cExpression targets corresponds to the quantification type in hand (i.e. number of exons at exon-level).