CSF1 and neoplasm: Our preclinical studies showed that in the OSCC cells, the ectopic TWIST1 overexpression increased CSF1 expression while TWIST1 gene silencing down-regulated CSF1. To clarify the diversity of macrophage recruitment within the tumor and their relevance for invasiveness, we confirmed the potency of OSCC-induced TWIST1 expression to promote macrophage chemotaxis using the in vivo Matrigel plug assay, supporting that TWIST1-CSF1 axis impacts on remodeling of OSCC microenvironment via recruitment and polarization of TAMs to promote pro-metastasis signaling.