BRCA1 and BRCA2 genes are known for their association with hereditary breast and ovarian cancer. These genes play a key role in maintaining genome stability and are involved in the repair of damaged DNA. Mutations in the BRCA1 and BRCA2 genes can disrupt the normal functioning of these proteins, leading to an increased risk of developing breast and ovarian cancer. Individuals with a family history of these types of cancer or those who carry known pathogenic variants in these genes may benefit from genetic testing. A variety of multigene panels can identify mutations in BRCA1 and BRCA2, helping to assess risk and inform treatment decisions. For individuals identified as carriers of pathogenic BRCA1 or BRCA2 variants, personalized treatment strategies can be implemented. Surgery plays a key role in the treatment of BRCA1 and BRCA2 breast and ovarian cancers, while platinum-based chemotherapy is often the first-line choice of adjuvant and neoadjuvant treatment. Additional chemotherapy drugs, such as taxanes, can be combined with platinum drugs to improve treatment outcomes, and targeted therapies, particularly PARP inhibitors, exploit DNA repair defects caused by BRCA mutations, leading to selective killing of cancer cells. The aim of this paper is to provide a comprehensive explanation regarding the nature of the BRCA1 and BRCA2 genes, elucidating the mechanisms behind their mutation and to state the contrasting characteristics of hereditary and sporadic variants of related cancers.