This suggests that while miR-346 may contribute to progression of early-stage PC (through upregulation of YWHAZ and AR activity), miR-197 and -361-3p may act at the castrate-resistant stage of the disease to promote or maintain resistance to AR-targetting therapies, through downregulation of tumour-suppressive targets and stabilisation of AR transcript. The gene discussed is AR; the disease is neoplasm.