The medical management of inflammatory bowel disease (IBD) has changed considerably since the advent of biological and molecular targeted therapy. The anti-TNF-α monoclonal antibody infliximab was FDA-approved in 1998 as the first targeted therapy for moderate to severe Crohn’s disease (CD). Since then, targeted therapies aimed at the particular pathways involved in the development of IBD are increasingly being developed and investigated. Promising novel therapeutic classes include the anti-IL-12/23 and anti-IFN-agents and the selective adhesion molecule inhibitors. 1 In volume 12, number 11 (2006) of Inflammatory Bowel Diseases, Magro and Costa2 presented an intriguing case report, describing a patient with chronic active CD and chronic myeloid leukemia (CML) who remained asymptomatic for more than 3 years while under molecular targeted therapy with imatinib, despite the interruption of prednisolone and mesalamine at the patients own initiative. Within this period the inflammatory parameters also changed to normal levels. These results led to the assumption that the sustained CD remission was caused by the small molecule receptor tyrosine kinase (RTK) inhibitor imatinib.