We have lived through amazing times in rheumatology, with progress in drug discovery based on intuition (eg, gold, sulfasalazine) to discovery driven by advances in understanding of the molecular basis of disease pathogenesis and application of technology, chiefly based on molecular biology and immunology. When we were medical students autoimmunity was a vague concept, inflammatory mediators were a few small chemicals, cellular signaling was a mystery, and therapeutics was dominated by the organic medicinal chemists. Rheumatoid arthritis (RA) was an incurable, painful, life-damaging, and life-shortening disease (1) for which prior attempts at a cure, as with the lauded discovery of corticosteroids, ended lamentably (2). But through empiricism, there was progress, even without access to modern technological tools. There has been considerable further progress, with breakthroughs in the understanding of cellular immunology and hence autoimmunity, the molecular biology “revolution” enabling cloning of complementary DNAs encoding messenger RNAs (mRNAs) for active mediators of immunity and inflammation, and, subsequently, the generation of pure proteins (3). The discovery of therapeutic monoclonal antibodies—first in mice and then by reducing their immunogenicity, converting them closer to human antibodies—was pivotal (4). Now there are many