Indeed, while targeting HDAC6 has shown promise in preclinical models of ADPKD as described above, HDAC6-null mice with hyperacetylated α-tubulin are viable and develop normally (Zhang et al., 2008), suggesting that disease-selective targeting of the microtubule network might be possible to achieve while limiting undesirable toxicity. This evidence concerns the gene HDAC6 and autosomal dominant polycystic kidney disease.