CRC in IBD patients is thought to be preceded by unequivocal neoplastic epithelial changes known as dysplasia. Early detection of dysplasia is a primary goal of endoscopic surveillance. Riddell and colleagues described a classification system of no dysplasia, indefinite for dysplasia, low-grade dysplasia (LGD), and high-grade dysplasia (HGD) that is still used today[,]. When the pathologist cannot distinguish between dysplastic and non-dysplastic atypia or inflammatory-associated changes, the sample is considered indefinite for dysplasia. LGD and HGD are differentiated based on the distribution of nuclei within the mucosa[]. There is high inter-observer variability in grading dysplasia among even experienced gastrointestinal pathologists, so guidelines recommend all cases of suspected dysplasia be reviewed by a second gastrointestinal pathologist[,]. All dysplasia should be defined as invisible if obtained by random biopsies or visible if identified and removed or sampled by targeted biopsies[]. Furthermore, visible lesions should be classified by the endoscopist as polypoid or non-polypoid, as per the Paris classification[,]., There is no single test to confirm a Crohn’s diagnosis, and Crohn’s disease symptoms are often similar to other conditions, including bacterial infection. Your healthcare providers should evaluate your current medical history and use information from diagnostic testing to exclude other potential causes of your symptoms., Advancements in CRC screening and surveillance and improved treatment of IBD has reduced CRC incidence in patients with ulcerative colitis and Crohn’s colitis. Most cases of CRC are thought to arise from dysplasia, and recent evidence suggests that the majority of dysplastic lesions in patients with IBD are visible, in part thanks to .