Because S1PR3 levels are elevated in a series of human lung adenocarcinoma cell lines, Zhao et al. [99] found that TGF-β-stimulated S1PR3 upregulation boosts the proliferation of human lung adenocarcinoma cells in mice through the TGF-β/SMAD3 pathway; in contrast, knockdown of S1PR3 markedly blocks tumor growth and lung metastasis. The gene discussed is SMAD3; the disease is lung adenocarcinoma.