In addition, functional enrichment analysis showed that CSF3R is involved in key pathways, such as cytokine-receptor interactions and JAK-STAT signaling, which is in line with previous studies, where STAT3 activation has been shown to exacerbate the DSS-induced UC model in IBD, and JAK/STAT signaling has been associated with the progression of colitis [26–28], and the role of JAK inhibitors, such as tofacitibib, in the treatment of ulcerative colitis (UC) as evidenced by the clinical efficacy of JAK inhibitors, such as tofacitib [29]. This evidence concerns the gene CSF3R and colitis.