Upon replication stress, replication forks stalland prolong cell-cycle arrest allowing time for DNA repair and re-entry intothe cell cycle.65 Damage to replication fork protection evokesgenomic instability and tumorigenesis.66 Treatment resistancepromotes cancer cell progression through the cell cycle in the presence ofDNA damage and replication stress; these include alterations inRAD51,67PTIP, Chromodomain Helicase DNA Binding Protein 4(CHD4), and the FA repair pathway.65Downregulation of these factors in BRCA1/2-deficient cellsleads to forkhead protection and PARPi resistance. This evidence concerns the gene BRCA1 and cancer.