RAD51 and ovarian cancer: Many reports support the notion that DSBs arising from ssDNA gaps are repaired by RAD51 in HRP cells.[14, 16, 56] DHS induced downregulation of RAD51 expression and HRR (Figures 1 and 3), which may further assist in accumulating collapsed/damaged replication forks (Figure 8J,K; Figures S42 and S43, Supporting Information), leading to accumulation of DNA damage and sensitization of ovarian cancers (Figures S42–S47, Supporting Information) and other types of cancers (Figures S48–S50, Supporting Information).