Although a considerable element of heritable gene expression is proposed to act in trans, trans-eQTL have proved difficult to define in the cell populations studied to date. It is probable that trans-acting variants are involved in a more multifactorial process than those acting in cis, reflecting contributions both of prevailing environmental cues and the cellular context. We explored this question in each of our primary cell populations and mapped trans associated eSNPs using a conservative significance threshold of 1×10−11, based on a Bonferonni correction given the number of SNPs analysed. For autosomal genes and SNPs, we identified 1704 eSNPs involving 75 genes specific to B-cells, 101 to monocytes and 19 shared (Figure 1, Supplementary Table 2). It is increasingly apparent that particular variants act as master regulators of transcription as trans-eQTL12,14. Many of these eSNPs form cis-eQTL to genes that probably define the nodal gene of these subsets (Supplementary Table 2, Supplementary Figure 6) and we observe two highly cell specific examples in the form of KLF4 (Supplementary Figures 7,8) and LYZ (discussed below). We found that only 7% of
