Accumulating evidence from studies in both cell cultures and ALS animal models suggests that the pro-inflammatory cytokine, tumor necrosis factor-α (TNF-α), may participate in the death of MNs, even from the early pathogenic events of the neurodegenerative process.36, 37 Both serum TNF-α and its soluble receptors have been reported to be significantly higher in ALS patients compared with healthy controls.38 Moreover, TNF-α impairs skeletal muscle trophism. The gene discussed is TNF; the disease is Melnick-Needles syndrome.