High glucose flux into the HBP is associated with insulin resistance, impaired glucose tolerance and type 2 diabetes,30 effects which could be linked to increased GFPT2 activity.31, 32 Notably, C5a influences glucose metabolism in neutrophils, leading to increased glucose uptake and glycolysis, thus resembling insulin action in these cells.33, 34 Moreover, C5aR1 contributes to insulin resistance in an in vivo obesity model.35 These data imply that complement, and in particular the C5a/C5aR1 axis, might affect glucose metabolism not only in immune cells but also in osteoblasts. The gene discussed is C5AR1; the disease is obesity due to melanocortin 4 receptor deficiency.