The production of CRP occurs almost exclusively in the liver by the hepatocytes as part of the acute phase response upon stimulation by IL-6, TNF-αand IL-1-βoriginating at the site of inflammation. Its short half-life makes CRP a valuable marker to detect and follow up disease activity in Crohn's disease (CD). In contrast, ulcerative colitis has only a modest to absent CRP response despite active inflammation, and the reason for this is unknown. In CD, serum levels of CRP correlate well with disease activity and with other markers of inflammation as the CDAI, serum amyloid, IL-6 and faecal calprotectin. CRP is a valuable marker for predicting the outcome of certain diseases as coronary heart disease and haematological malignancies. An increased CRP (>45 mg/L) in patients with IBD predicts with a high certainty the need for colectomy and this by reflecting severe ongoing and uncontrollable inflammation in the gut. Finally, trials with anti-TNF and anti-adhesion molecules have shown that a high CRP predicts better response to these drugs. However, whether we need to include CRP as an inclusion criterion for future trials with biologicals is still a matter of debate.