TDAG51 deficiency reduces cell death in atherosclerotic lesions and peritoneal macrophages. TDAG51−/−/ApoE−/− (dKO) or ApoE−/− mice were placed on control chow diet for 25 weeks. A, Representative images of atherosclerotic lesions from 5 mice per group were stained for TUNEL and cleaved caspase‐3. Microscope magnification ×20. B, Peritoneal macrophages isolated from wild‐type C57BL/6 (C57) mice or TDAG51−/− mice were treated with 2.5 μg/mL tunicamycin (Tm), 100 nmol/L thapsigargin (Tg), or 10 μmol/L 7‐ketocholesterol (7‐KC) for 24 hours. Cytotoxicity was determined by measuring LDH release. Mean±SE from 5 independent experiments are shown. *P<0.05 relative to C57 controls. C, Negative controls for IHC sections. Primary antibodies were omitted, and only secondary antibodies were used (anti‐mouse, anti‐rat, or anti‐rabbit, with heat‐induced epitope retrieval [HIER] where specified). Negative control for the TUNEL staining had no terminal deoxynucleotidyl transferase (TdT) added to the staining mixture. TDAG51 indicates T‐cell death‐associated gene 51; ApoE, apolipoprotein E; dKO, double knockout; LDH, lactate dehydrogenase; IHC, immunohistochemistry; PPARγ, peroxisome proliferator‐activated receptor γ; ab, antibody; NT, nontreated.