It has been reported that the expression of Hsp90 and its client proteins (e.g., EGFR, AKT, Raf-1, HER2, and CDK4/6), which are closely related to the development and progression of tumors, is increased [38] and that the inhibition of Hsp90 function leads to the degradation of tumor-associated client proteins [39]. The gene discussed is CDK4; the disease is neoplasm.