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). This evidence concerns the gene RAD51 and cancer.