Ichthyosis vulgaris (IV) – a dry flaky skin condition frequently seen by all dermatologists – is arguably the most common monogenic hereditary skin disorder.1 Despite there being a body of biochemical and genetic mapping literature dating from the 1980s suggesting that some kind of defect in the skin barrier protein filaggrin might be involved in the pathophysiology of IV, no genetic defect had been identified to confirm or disconfirm this until some 20 years later. This evidence concerns the gene FLG and ichthyosis vulgaris.