These data, coupled with the limited weight lossand the regulation of neutrophil recruitment upon Hdac6 depletion demonstrated in the same study, further depict HDAC6 asa key regulator in several secondary phenotypes associated with impairedCFTR function and support the potential benefits of using HDAC6-selectiveinhibitors in CF patients independently of CFTR phenotype. Here, CFTR is linked to cystic fibrosis.