The interruption of CCL2 inhibition leads to an overshoot of metastases and accelerates death due to monocyte release from the bone marrow and enhancement of tumour cell mobilization from the primary site, as well as blood vessel formation and increased proliferation of metastatic tumour cells in the lungs in an IL-6- and VEGF-A-dependent manner [268]. This evidence concerns the gene IL6 and neoplasm.