BCL2 and infection: SAG (sensitive to apoptosis gene) is recently reported to be a key regulator of immune overactivation and protumorigenesis.11 Under an infection condition, SAG-dependent ubiquitin–proteasome system (UPS) ubiquitinates the proapoptotic Bax and SARM (sterile α and HEAT/armadillo-motif-containing protein) but not antiapoptotic Bcl-2, hence providing survival advantage to macrophages to fight the infection.