While the anti-atherogenic effects of ABT-263 are encouraging, macrophage deficiency of BCL2 increases their apoptosis in atherosclerosis,32 and monocyte/macrophage apoptosis reduces plaque development,27 such that agents that target BCL2/BCLXL such as ABT-263 might act by removing macrophages or other leucocytes, and not just through removing senescent cells. Here, BCL2L1 is linked to atherosclerosis.