As both CRPCs and ER− BCas (i.e., TNBC and ER−/HER2+ BCa, or even ER+ BCas that become resistant to hormone therapy) are refractory or unresponsive to hormone therapy, a better understanding of roles of AR and WNT pathways and their interactions in these hormone-refractory diseases should open a new avenue for improving their treatment and for combating the inevitable challenge of therapy resistance. The gene discussed is AR; the disease is glycogen storage disease VI.