To explore the mechanisms by which inactivation of S1PR1 expression in BM-derived myeloid cells, including macrophages, accelerated the accumulation of apoptotic nuclei in atherosclerotic plaques of BM transplanted and HF diet-fed Ldlr KO mice, we examined the effects of treatment of primary mouse macrophages with SEW2871, a selective S1PR1 agonist [33], on apoptosis induced by either tunicamycin, an inhibitor of protein glycosylation that induces apoptosis secondary to ER-stress, and oxLDL, an inducer of oxidative stress [9,10,17,18]. This evidence concerns the gene S1PR1 and hydrops fetalis.