The impaired IL10 signalling pathway observed in IL10 receptor deficiency, the underlying pathophysiological cause of a proportion of very early onset inflammatory bowel diseases, as well as the STAT3 deficiency characterising Job syndrome and resulting from loss of function mutations in STAT3, are both involved in the malignant transformation of B lymphoid cells, presumably by compromising the physiological homeostasis of B-cell precursors [17,18]. Here, STAT3 is linked to inflammatory bowel disease.