Of note, depletion of the endogenous SF3B1 or SF3B3 partially inhibited the apoptosis induced by JA in breast cancer cells, while the simultaneous knock-down of SF3B1 and SF3B3 completely abrogated the apoptotic effects of JA, suggesting that both SF3B1 and SF3B3 are required for the antitumor activity of JA in breast cancer cells. Here, SF3B1 is linked to breast carcinoma.