We found previously that high baseline LPS activity in sera of Finnish patients with T1D, even though normoalbuminuric, is associated with the progression of DN.1 This, together with the potential antiapoptotic role of PDK1, led us to hypothesize that serum LPS could reduce the expression of PDK1 and induce podocyte injury and thereby contribute to the development of DN. The gene discussed is PDK1; the disease is type 1 diabetes mellitus.