Presumably, this immune normalization may be attributed to the dual role of chemokines that recruit both antitumor immune cells and protumor immune cells [32], as in our spatial profiling, hot tumors exhibited the highest expression levels of CCL5, CXCL9, CXCL10, CXCL11, CCL2, CXCL12 and CCL20, wherein CD8 + T cells can be recruited by CCL5, CXCL9, CXCL10 and CXCL11, but CCL5 can also recruit tumor-associated macrophages, which can also be recruited by CCL2 and CXCL12 [40–44], while Tregs are recruited by CCL20 [43, 45, 46]. Here, CCL2 is linked to neoplasm.