“…Though this may be an adaptive epiphenomenon, it cannot be excluded that this finding indeed reflects the increased proliferative pressure exerted by various inflammation-related factors on residual colonic stem cells. The development of carcinoid as a ‘reactive’ process to the chronic mucosal damage induced by ulcerative colitis is also indirectly supported by the following features: long previous history of ulcerative colitis (more than 5 years in 72% of subjects) [3,4,5,6,7,8, 10, 11, 14, 15], multifocal distribution in ulcerative colitis-affected mucosa (33% of the cases) [3, 4, 7, 13, 15, 16], concomitant development of colorectal dysplasia or adenocarcinoma (28% of the cases) [3, 4, 6, 13]. …”