GPER agonists could modulate the fibrovascular stroma of PDAC to increase vascular density and perfusion by reducing overall solid stress (through collagen and FN) which would increase intratumoral drug perfusion, while concurrently impeding the adaptive fitness of tumor and stromal cells to survive under hypoxic conditions (via HIF‐1A) and thus promoting widespread hypoxic necrosis. The gene discussed is FN1; the disease is neoplasm.