In a model of breast cancer, Huang et al.13 showed an increase in PGE2 levels and cell proliferation downstream of Caspase-3 activation upon apoptosis induction, and that there was reduced AA release, PGE2 production and cell proliferation in Casp3−/− cells which could be rescued by overexpression of iPLA2 (514–806). The gene discussed is CASP3; the disease is breast cancer.