However, dysregulation of homeostasis in digestive inflammation, as exemplified by ulcerative colitis and Crohn’s disease, tips the differentiation of macrophages towards the classically activated M1-like CD11chiCX3-chemokine receptor 1-positive (CX3CR1+) cell phenotype by tumor necrosis factor (TNF) and interleukin (IL)-23 [3,4]. This evidence concerns the gene TNF and Crohn disease.