Thus, the authors of this very interesting study also suggested that, simply, the loss or inhibition of HDAC6′s deacetylating function attenuated bleomycin-induced lung fibrosis by hyperacetylating target proteins, whereas in Hdac6(−/−) knockout mice, the additional loss of HDAC6 function to transport cytotoxic polyubiquitinated (misfolded) proteins into autophagosomes for their degradation, may aggravate bleomycin-induced lung fibrosis by causing defective autophagy [235]. The gene discussed is HDAC6; the disease is pulmonary fibrosis.