Possibly due to the disruption of VEGFR1 signaling in concert with the downregulation of other angiogenic and growth regulatory molecules ERbB4, FGFR3/4, c-RET, CXCL16, TSP-1, IGFBP3 and IL-8, we observed disrupted intratumoral and tumor surrounding stromal vasculature, capillary tube formation and hence halted HNSCC progression. The gene discussed is CXCL16; the disease is neoplasm.