However, remarkable heterogeneity in the mutational spectrum, copy number alterations, transcriptomes and epigenomes within and between primary tumors, circulating and disseminated tumor cells and metastases have been revealed through high-throughput molecular profiling studies, and the notion that hormone receptor and HER2 status may differ significantly between metastases and primary tumors has been validated in several studies [7–12]. This evidence concerns the gene NR4A1 and neoplasm.