(42) shed some light into the molecular mechanism that breast-cancer cells use to reprogram the TGFβ antiproliferative signaling and to promote EMT and metastasis; the results indicate that YWHAZ (14-3-3ζ) activation is key to overcoming the cytostatic effect of TGFβ because it blocks the p53/SMAD association and induces GLI2/SMAD interaction in breast cancer bone metastasis. Here, GLI2 is linked to breast cancer.