Ataxia-telangiectasia (A-T) is a disorder where patients are unable to use ataxia-telangiectasia, mutated (ATM) to recognize and initiate DNA repair. We examined the effects of ionizing radiation (IR) on normal and A-T lymphoblastoid cell lines (LCLs) on apoptosis. LCLs were irradiated to damage DNA, incubated and collected to chronicle the effects of IR on apoptosis, with or without Protein Phosphatase 2A (PP2A) inhibitor okadaic acid (OA). Through the TUNEL assay, normal LCLs exhibited the highest apoptotic activity on day 1 following IR treatment, whereas A-T LCLs demonstrated no significant apoptotic response. Our findings suggest that ATM was responsible for the rapid response to double-stranded breaks (DSB). Preliminary results suggested that normal LCLs treated with OA, with or without IR, exhibited significantly decreased apoptotic activity when compared to normal LCLs treated with IR only. These results proposed that PP2A activity was necessary for the proper function of the IR-induced apoptotic pathway.