One class of recurrent ESR1 fusion transcripts have been found in a subset of Luminal B primary breast tumors that retain the first two non-coding exons of ESR1 (ESR1-e2) fused to various sequences from a nearby gene, coiled-coil domain containing 170, CCDC170 (ESR1-e2>CCDC170), potentially generated by tandem-duplication, based on the observed orientation of the fusion sequences.2 This fusion gene forms a promoter trap driving aberrant expression of CCDC170 since this gene is now in the context of the ESR1 promoter, producing stable truncated forms of CCDC170 protein (ΔCCDC170). The gene discussed is ESR1; the disease is breast neoplasm.