This was presumably triggered by the (i) detection of a causal relationship between antithrombotic thrombomodulin fragments and the cytoprotective effect on vascular endothelial cells, (ii) by the inhibition of tumor growth by silencing of GPR15 [53], (iii) by its role in skin diseases, and (iv) by its role for homeostasis in the colon, the organ interacting with the majority of intestinal microbiota. The gene discussed is GPR15; the disease is neoplasm.