Moreover, we predicted that if derepression of DAF-16 is sufficient to instigate its immune function then the degree of pathogen resistance conferred by disrupting the insulin receptor should be invariant over the worm’s lifespan such that upon infection daf-2 L4 animals and older post-reproductive daf-2 worms would experience an equivalent survival advantage relative to their wildtype counterparts. The gene discussed is INSR; the disease is infection.