C5 and neoplasm: In a colorectal cancer model, PSGL-1 on TAM could bind to P-selectin and activate the JAK/STAT1 pathway, inducing the transcription of C5 and the release of C5a, which shifted the TAM to the M2 phenotype-mediated tumor-suppressor microenvironment, and that the blockade of PSGL − 1 significantly reduced the growth of colorectal cancer [88].