We demonstrate cellular insulin resistance with a functional glucose uptake assay as well as reductions in Akt phosphorylation, supporting that lumican mediates its effects on adipocyte insulin resistance at least in part via an Akt-related mechanism, but our data cannot rule out other mechanisms of lumican-mediated insulin resistance in addition to Akt Ser473 phosphorylation, including regulation of other insulin signalling mediators or GLUT4 translocation. The gene discussed is AKT1; the disease is Insulin resistance.