Moreover, we found a novel clinic-related mechanism for combating breast cancer resistance to paclitaxel, which implies that S-72 restores multipolar spindle formation and causes deadly chromosomal instability in MCF7/T cells by reducing STING signals, and STING suppression further sensitizes MCF7/T cells to paclitaxel and S-72. The gene discussed is STING1; the disease is breast cancer.