MCL1 and neoplasm: The active form FTY720‐P, a functional antagonist of S1PR1, can restrain tumor growth via various S1PR1‐dependent mechanisms: (1) suppressing proapoptotic Bim and enhancing pro‐survival Mcl‐1 proteins58; (2) disrupting the S1P/SphK1/S1PR1 positive feedback loop for sustained NF‐kB and STAT3 activation within the breast tumor microenvironment,13 crucial for TNBC progression; (3) Nuclear FTY720‐P also acts as a potent inhibitor of class I HDACs, and sensitizes breast cancer cells to tamoxifen therapy.24