through the S1PR1-STAT3 signaling pathway, resulting in a microenvironment suitable for tumor growth before the arrival of CTCs.111 Additionally, CCL2 can recruit TAMs and Tregs, stimulating angiogenesis, inhibiting immune cell function, and promoting PMN establishment in the lung.112 Within the PMN, host stromal cells might enhance the expression of inflammatory factors following stimulation by TDSFs. This evidence concerns the gene STAT3 and neoplasm.