This mechanistic crosstalk among tissue factor, VEGF, PD‐L1, and TMEM176B highlights how our dual‐targeted approach can recalibrate multiple pro‐cancer circuits at once, blunting the coagulation and angiogenic factors that feed tumor growth and metastasis, while concurrently lifting immune checkpoints that tumors exploit for survival. The gene discussed is VEGFA; the disease is neoplasm.