For instance, structure-based inhibitors such as DDO-5936 and DDO-5994 were shown to selectively degrade Cdk4 and other kinase clients in cancer cells without broadly impacting the rest of the Hsp90 proteome.54,55 This selective cytotoxicity toward tumor-specific signaling networks underscores the potential of Hsp90–Cdc37 disruptors to achieve cancer cell-specific inhibition with minimal systemic toxicity, representing a significant advancement in the development of safer, more precise chaperone-targeted therapies. This evidence concerns the gene CDK4 and neoplasm.