“…Blocking the interaction of CD63 with its endogenous ligand TIMP1 34 might be exploited to deplete FLC stem cell populations by disrupting stem cell maintenance mechanisms. 36 Drugs that inhibit YAP1, 37,45 AREG, 46,47 CTGF, 30,31 and/or cysteine-rich angiogenic inducer 61 (CYR61) 48,49 could be engineered to bind to CD63, thereby targeting their delivery to FLC cells to reduce tumor growth, metastasis, and desmoplasia. Finally, MSLN has been successfully targeted by CAR-T cells and other immunotherapies in ovarian cancer, 50e52 suggesting another novel, and more personalized, therapeutic strategy that might be applied to FLC.…”