Previous studies in apoE knockout mice and scavenger receptor BI knockout mice have highlighted that changes in tissue lipid levels as a result of the genetic hyperlipidemia can underlie the development of pathological skin phenotypes, i.e. disrupt epidermal layer organization and impair skin barrier function and/or induce the accumulation of inflammatory cells such as macrophages and T cells11–13. The gene discussed is APOE; the disease is hyperlipidemia.