Together, the results support the notion that hepatocyte response to Plasmodium in vitro infection entails two distinct apoptosis mechanisms: (1) an HGF-stimulated mitochondrial-independent response that preferably targets hepatocytes harboring early liver schizonts and (2) a Fas-mediated mitochondrial-dependent apoptosis mechanism, acting on both infected and non-infected hepatocytes. The gene discussed is FAS; the disease is infection.