As a consequence, Gal-CC were more invasive and metastatic in vivo and were able to modulate the immune infiltrating cell profile at early and late times post-injection, attracting fewer immune cells during the early stages of extravasation, while at later times promoting the accumulation of pro-tumor immune cells, specifically TAMs, which facilitate establishment of the niche and TME. The gene discussed is CXCR1; the disease is neoplasm.