For example, in Idiopathic Pulmonary Fibrosis (IPF), inhibition of Hsp90 is a promising strategy at the late stage of the disease [45], whereas in CF benzoquinone ansamysin molecules that inhibit this Hsp block the maturation of nascent CFTR and strongly accelerate its degradation by the proteasome [34], a phenomenon which depends on Hsp90 co-chaperone partner Aha I (Activator of Hsp90 ATPase activity). This evidence concerns the gene CFTR and cystic fibrosis.