Based on the correlation between cancer cell line sensitivity to TRPS1 knockout and ESR1 knockout (Fig 1B), the enrichment of an ER binding motif in both increased and decreased ATAC-seq peaks (Fig 3D), and the over-representation of estrogen response gene sets in the genes repressed by TRPS1 depletion (Fig 4D), we focused on ER target genes to explore a possible mechanism by which TRPS1 indirectly activates transcription. The gene discussed is ESR1; the disease is cancer.