HSP90AB1 and cancer: The CDK4 downregulation by NDNB1182 provides a logical mechanistic connection from Hsp90β inhibition to ERV and IFIT overexpression, because CDK4 is a client for Hsp90β and it is known that CDK4/6 inhibition can reactivate ERV expression and interferon response in cancer cells through downregulating DNMT1 expression and DNA methylation (53).