We previously showed that BT474 breast cancer cells (luminal B; ER+/PR+/ERBB2+) superinduce selected SUMO-sensitive (activated) PR target genes upon progestin treatment relative to other PR+ cell line models, presumably because kinase pathways downstream of HER2 (i.e., MAPKs) input to persistent PR Ser294 phosphorylation [32]. The gene discussed is ERBB2; the disease is breast carcinoma.