Others have shown that KRASG12D-mediated repression of IRF2 subsequently enhanced the expression of CXCL3 that binds to CXCR2 on myeloid-derived suppressor cells (MDSCs) and increases the migration of MDSCs to the CRC microenvironment, which results in higher IRF2 expression and more sensitive response to anti-PD-1 therapy in vivo[9]. The gene discussed is CXCR2; the disease is colorectal carcinoma.