For example, combination therapy using emodin and doxorubicin sensitize breast cancer cells to doxorubicin by inhibition of proliferation in the DNA damage pathway (decreasing the levels of X-ray repair cross complementing 1 (XRCC1), poly(ADP-ribose) polymerase 1 (PARP1) and RAD51 proteins) and by downregulation of the expression of AKT1 and enhancement of the expression of p53 [67]. The gene discussed is XRCC1; the disease is breast carcinoma.