Overexpression of matrix-metalloproteinases (MMPs), proteases that degrade an array of matrix molecules, in the inflamed synovium has been long known, and more recent data points to overexpression of tenascin-C (TNC), an endogenous TLR4 agonist, being a key driver of RA chronicity (Midwood et al, 2009; Aungier et al, 2019). The gene discussed is TNC; the disease is rheumatoid arthritis.