Anti-angiogenic drugs make tumor cells achieve a hypoxic state by inhibiting tumor angiogenesis, causing DNA damage in tumor cells, and the most characteristic feature is DNA DSB; at this time, DNA replication pressure increases, and then the expression of HRR pathway-related proteins, such as RAD51 and BRCA1/2, is down-regulated through various ways, and the final result is HRR defects. This evidence concerns the gene BRCA1 and neoplasm.