The rapid cold-hardening (RCH) response increases the cold tolerance of insects by protecting against non-freezing, cold-shock injury. Apoptosis, or programmed cell death, plays important roles in development and in the elimination of sub-lethally damaged cells. Therefore, our objectives were to determine whether apoptosis played a role in cold-shock injury and, if so, whether the RCH response prevents this cold-induced apoptosis in Drosophila melanogaster. RCH increased the cold tolerance of the adults at the organismal level. No flies in the cold-shocked group survived direct exposure to -7°C for 2 h, whereas significantly more flies in the RCH group survived exposure to -7°C for 2 h after a 2-h exposure to -7°C. At the cellular level, we used a TUNEL assay to detect and quantify apoptotic cell death in control, cold-shocked, RCH, heat-shocked (37.5°C, 30 min), and frozen (-20°C, 24 h) groups. Overall, we found that apoptosis can be induced by temperature stresses including cold-shock, heat-shock as well as freezing, and that the RCH response improves cellular viability by blocking cold-induced apoptosis. This research is supported by NSF grant #IOB-0416720.