CCL2 was also found to upregulate PD-L1 expression through transglutaminase 2 (TG2)-mediated stabilization, as by Choi et al. (2020), which then resulted in a dual mechanism of resistance: tumor cell surface retention of PD-L1 protein enhanced by TG2, and CCL2 recruitment of immunosuppressive PD-L1 TAMS likely strengthening this immune evasion [29]. Here, CCL2 is linked to neoplasm.