While hormone receptor expression (18–20) and the presence of chromosomal rearrangements, such as JAZF1-SUZ12 and JAZF1-PHF1 fusions (21), have been implicated in the pathogenesis of LG-ESS, the specific cellular subpopulations responsible for tumor initiation, progression, and recurrence have not been comprehensively characterized. This evidence concerns the gene NR4A1 and neoplasm.