Regarding the human coronaviruses, ex-vivo experiments have demonstrated that upon SARS-CoV infection, viral 7a protein directly interacts and forms a complex with antiapoptotic Bcl-XL protein and other prosurvival factors (Bcl-2, Mcl-1, and A1), promoting apoptosis in a caspase-3 dependent manner [121]. The gene discussed is BCL2L1; the disease is severe acute respiratory syndrome.