A previous study demonstrated that CCDC170 was fused to ESR1 and employed the constitutively active ESR1 promoter to induce the expression of a truncated form of CCDC170. The fused gene was enriched in luminal B breast tumors and was found to promote a more aggressive phenotype by enhancing cell migration, invasion, anchorage-independent growth and endocrine therapy resistance [7]. This evidence concerns the gene ESR1 and breast neoplasm.