Similar effects were demonstrated for a TNF-α antagonist being more efficient in patients with increased inflammatory markers.11 However, based on the hypothesis of chronic, subthreshold inflammation in TRD that may well be present at the level of microglial activation even without measurable traces in the periphery, also patients without significantly elevated peripheral inflammation may have exhibited a minocycline-targetable central inflammation and might thus have responded to minocycline treatment. The gene discussed is TNF; the disease is treatment resistant depression.