Emerging evidence suggests that the intracystic environment in PLD is not immunologically neutral but rather characterized by chronic, cytokine-rich inflammation and dysregulated cholangiocyte signaling, including interleukin-6/interleukin-8 and vascular endothelial growth factor pathways.14,15) Conceptually, such a milieu—together with cyst stasis, intermittent hemorrhage, and relative hypoxia—could provide “fertile soil” that facilitates survival and proliferation of E. histolytica once trophozoites reach the liver via the portal circulation. The gene discussed is VEGFA; the disease is cyst.