The N-terminal domain Hsp90 inhibitors could promote the lysosomal degradation of oncogenic ATPase MORC2 through the disruption of its homodimer formation, thereby suppressing MORC2-driven breast cancer progression [104]; in addition, disrupting the interaction between Hsp90 and PGK1, and reducing GSK3β expression, resulted in a significantly reduced inhibition of β-catenin expression to maintain the stemness of breast cancer stem cells [98]. This evidence concerns the gene HSP90AA1 and breast carcinoma.