In an animal model of colitis, the inhibition of platelet function by selective deletion of COX-1 in platelets (which recapitulated the human pharmacodynamics of low-dose Aspirin, i.e., suppression of platelet TXA2 production associated with substantial sparing of the systemic prostanoid biosynthesis) ameliorates colitis symptoms, chronic intestinal inflammation, and fibrosis (Sacco et al., 2019) (Figure 2). The gene discussed is PTGS1; the disease is colitis.