Our results signify that while impediment of p53-SMAR1 loop induced VEGF expression in NLCSC cells thereby favoring endothelial cell (EC) migration and network formation in tumor environment, reframing of these pro-angiogenic signals by capsaicin blocked VEGF production even under hypoxic condition, thereby restraining NSCLC-induced net work formation by the endothelial cells. The gene discussed is TP53; the disease is non-small cell lung carcinoma.