Additionally, our work shows that decreasing the expression of S1PR1 using the selective antagonist BAF312 dramatically inhibits STAT3 activity and promotes apoptosis in breast cancer cells, which is consistent with previous research results showing that S1PR1 could help activate STAT3 and that activated STAT3 greatly elevates the expression of VEGF and suppresses the expression of Bax to evade apoptosis. This evidence concerns the gene S1PR1 and breast cancer.