In the present study, we find that BLM increases MIP-4, which suggests that initially BLM is inflammatory, and if BLM treatment persists as is the case of its use in neoplasm treatment, the secondary effect of BLM is lung fibrosis, and as this study indicates, MIP-4 may represent one mechanism through which BLM leads to lung fibrosis. Here, CCL18 is linked to neoplasm.