Our assessment of a potential triad involving SPARC-caspase 8-Bcl2 in regulating apoptosis was based on earlier observations that Bcl2 binds to caspase 8 to inhibit caspase 8-mediated apoptosis in Fas-resistant neuroblastomas [17]; reports of SPARC's ability to promote apoptosis by decreasing the ratio of Bcl2 and BAX in autosomal dominant polycystic kidney cells [27], together with our recent observations that decreasing SPARC expression by siRNA diminishes chemosensitivity [28] and that this effect is based on SPARC's ability to interact with caspase 8 to promote apoptosis [8]. The gene discussed is BCL2; the disease is neuroblastoma.