Chemical inhibition of RAD51 by the small-molecule inhibitor B02 or modulation of RAD51 expression both led to marked inhibition of MM cell survival in the absence of exogenous DNA damage and sensitized tumor cells to the topoisomerase II inhibitor doxorubicin and the alkylating agent melphalan through DSB induction and the subsequent blocking of HR repair [51,139,140]. Here, RAD51 is linked to neoplasm.