The present study provides preliminary evidence on the possible oncogenic role of AXL in IBD: the increased expression of AXL—possibly due to the downregulated expression of its microRNA regulator/s, such as miR-199a and miR-34a—along with malfunctioning of the negative regulation of inflammation points toward AXL indeed being an important player in bridging IBD and CRC. Here, AXL is linked to inflammatory bowel disease.