Emerging evidence indicates significant interplay between these two axes: CXCR3 and CXCR4 can form functional heterodimers on the cell surface, potentially altering their signaling properties [185,186], and in colorectal cancer cells, CXCR3 expression has been shown to prevent CXCR4 internalization, thereby sustaining and enhancing its pro-invasive signaling output [187]. Here, CXCR4 is linked to colorectal cancer.