Loss-of-function HDAC8 mutations cause Cornelia de Lange syndrome (CdLS), characterized by intellectual disability, well-defined facial features, upper limb anomalies and atypical growth, etc. HDAC8 mutation leads to increased acetylation of structural maintenance of chromosomes protein 3 (SMC3), a subunit of the cohesion complex, and inefficient dissolution of the ‘used’ cohesin complex released from chromatin in prophase and anaphase (Deardorff et al., 2012). The gene discussed is HDAC8; the disease is Cornelia de Lange syndrome.