In vivo administration of exosomes derived from S1P-treated murine breast cancer cells in a breast cancer allograft model markedly promoted tumor growth and heightened CD8 T cell exhaustion, whereas exosomes from TGFBR2-silenced, S1P-treated cells exerted the reverse effect, underscoring the pivotal role of the S1P-TGFBR2 axis in modulating the tumor microenvironment. The gene discussed is TGFBR2; the disease is breast carcinoma.