Corynespora Leaf Fall is an important disease affecting rubber tree in Asia and Africa, caused by the necrotrophic fungus Corynespora cassiicola . A small protein toxin, the cassiicolin, is suspected to play an important role in the early stages of the disease. To demonstrate its role and evaluate the possible involvement of other effectors, a deletion mutant targeting the cassiicolin gene Cas1 was created from the highly aggressive isolate CCP. Wild-type and deletion mutant were not found different in terms of mycelium growth, sporulation and germination. Deletion of the Cas1 gene induced a complete loss of virulence on two susceptible rubber clones, as demonstrated by controlled inoculations on non-detached leaves. However, the mutant strain conserved some residual virulence when inoculation was conducted on detached leaves, notably with longer incubation times or when the leaves were wounded. The average filtrate toxicity analyzed on a range of clones was found reduced in the mutant compared to the wild-type, but not suppressed. Our results demonstrate: 1) that cassiicolin is indeed a necrotrophic effector conferring virulence to the CCP isolate in specific rubber clones, and 2) that other effectors potentially associated with saprotrophy are responsible for the symptoms observed in senescing/wounded tissues.