By activating PAK2, we hypothesis that BTV may promote cell survival via the phosphorylation of caspase-7 (53), Bad and B-Cell CLL/Lymphoma 2 (Bcl-2) thereby blocking apoptosis (54), which could allow for the extending of the duration of virus replication within a cell. The gene discussed is BAD; the disease is B-cell chronic lymphocytic leukemia.