Breast cancer genome-wide association studies (GWAS) together with fine-mapping have identified one signal at 3p26 containing four genetic variants associated with increased risk. One variant maps to an enhancer element in estrogen receptor positive (ER+) breast cancer cells. Promoter capture HiC, CRISPRi-mediated enhancer repression and reporter assays indicate that this enhancer regulates BHLHE40 (basic helix-loop-helix family member E40) and the presence of the risk alleles reduces BHLHE40 expression. In addition to BHLHE40, we have also identified a novel long noncoding RNA (lncRNA; called BRIAR) in the region, which is an eQTL that colocalised with the GWAS signal in breast tumours from TCGA. Notably, the BRIAR promoter sits at the 5` end of an 11kb enhancer cluster exhibiting high H3K27ac signal, with binding sites for breast-specific transcription factors. Accessible chromatin (ATACseq) peaks called in 410 TCGA samples from 23 cancer types, showed this enhancer cluster is largely restricted to breast tumours, specifically ER+ subtypes. CRISPRi targeted to the BRIAR promoter (5` end) but not the 3`end of the enhancer cluster suppressed the entire 11kb H3K27ac signal resulting in reduced BHLHE40 expression. RNAseq on BRIAR or BHLHE40 knockdown cells identified two main pathways; activated proliferation and suppressed interferon response, mainly through repression of STAT1. Consistent with the activated proliferation pathway, BRIAR/BHLHE40 knockdown significantly increased 2D and 3D breast cancer cell growth. Moreover, previous studies showed that STAT1 deficient mice spontaneously develop ER+ breast cancer, suggesting that early modulation of the interferon response is a major contributor to breast cancer risk. Finally, low expression of BRIAR in ER+ tumours correlates with higher immune cell infiltration. In concordance with this, we observed that genes co-expressed with BRIAR in ER+ breast tumours are enriched in functions related with immune cell attraction and activation - ongoing functional studies are also investigating this link.