Indeed, we found that IL-1β downregulated all standard fibroblast activation markers examined (i.e., F-actin, α-SMA, and COL1A1) except COL3A1. Moreover, a previous study reported that matrix rigidity amplifies pulmonary fibrosis through a reduction in COX-2 signaling in pulmonary fibroblasts [9], whereas IL-1β increases COX-2 as reported here and elsewhere [35,55]. The gene discussed is ACTA1; the disease is pulmonary fibrosis.