On another, having previously observed that circulating sIL-6R is always present at molar concentrations well in excess of corresponding IL-6 in early arthritis sera (median 60 ng/ml) (3), we interpret the fact that surface gp130 apparently acts as a “gate-keeper” with respect to STAT-3 signaling on CD4+ T cells to implicate trans (rather than classical) signaling as its preferential mediator. The gene discussed is IL6R; the disease is arthritic joint disease.