The most likely explanation for this is that both chemotherapeutic agents and irradiation trigger damage-induced signals that lead to the activation of proapoptotic Bcl2 family members, such as Bax and Bak (Cartron et al, 2003; Kim et al, 2003), and subsequent mitochondria destabilisation that as we reported previously results in the unusual activation of caspase-8 in NSCLC H460 cells by an as yet unresolved mitochondria-dependent mechanism (Ferreira et al, 2000). Here, BAX is linked to non-small cell lung carcinoma.