X‑linked inhibitor‑of‑apoptosis protein (XIAP) associates with the cleaved form of CASP9. It does not influence pro‑caspase‑9 auto‑processing but inhibits the activity of processed caspase‑9 and then the activation of effector caspases within the apoptosome complex (Srinivasula SM et al. 2001; Bratton SB et al. 2001). BIR3 domain of XIAP binds IAP binding motif (IBM) at the amino terminus on the small subunit of CASP9, which becomes exposed after proteolytic processing of procaspase‑9 at Asp315 (Srinivasula SM et al. 2001). Furthermore, the C‑terminal extremity of BIR3 binds the dimer interface of CASP9, interfering with CASP9 dimerization and hiding the catalytic residue (Srinivasula SM et al. 2001, Shiozaki EN et al. 2003).