In CD, CSF3R enhances mucosal immune and inflammatory regulation by promoting neutrophil differentiation and IL-17 signaling, which correlates with the activity of the antimicrobial peptide S100A9 and the IL-17 pathway [23]; whereas, in CAC, CSF3R signaling maintains neutrophil function and protects against bacterial invasion, epithelial repair, and IL-22/IL-23 production, and its absence exacerbates colitis and CAC susceptibility [24, 25]. Here, S100A9 is linked to colitis.