The likelihood that alternative mechanisms explain this bone frailty is evident in studies where human osteoblasts from healthy donors were treated with DMD patient sera (or wild‐type mouse calvariae were cultured with mdx mouse sera), which showed reduced mineralisation, downregulation of osteogenic and upregulation of pro‐osteoclastogenic cytokine mRNAs; the blunting of these changes by co‐incubation with an IL‐6‐neutralising antibody suggest IL‐6 is a vital bone loss mediator in DMD.37 This evidence concerns the gene IL6 and Duchenne muscular dystrophy.