Similarly, genetic inactivation of either Sr-b1 or Pdzk1 in bone marrow-derived cells increases atherosclerosis in mice, and knockout of either S1pr1, Sr-b1, or Pdzk1 in bone marrow-derived/myeloid cells increases apoptosis and necrotic core development within atherosclerotic plaques (5, 30, 48), consistent with the possibility that these three factors participate in the same pathway. Here, S1PR1 is linked to atherosclerosis.