Colorectal cancer (CRC) induces a systemic inflammatory response, possibly from proinflammatory cytokine production by colorectal tumor cells, the tumor microenvironment, or both.1 Systemic inflammatory response, as measured by markers including elevated C‐reactive protein (CRP), is linked to the poor prognosis of CRC.1 Evidence shows that the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway plays a role in the systemic inflammatory response in CRC.1, 2, 3, 4, 5, 6. This evidence concerns the gene SOAT1 and colorectal carcinoma.