Kontchou et al. recently showed that infected cells deficient in MCL-1, BCL-W, and BCL-XL, as well as cells pretreated with inhibitors targeting these pro-survival proteins, remained resistant to apoptosis induction, suggesting that these proteins are not essential to chlamydial evasion of host cell apoptosis, and that the loss of MCL-1 could be compensated for by other antiapoptotic mechanisms operating in tandem during chlamydial infection [124]. This evidence concerns the gene MCL1 and chlamydia trachomatis infectious disease.