TP53 and triple-negative breast carcinoma: Therefore, we expect that molecularly targeted therapies reactivating mutant p53 inactivation, such as eprenetapopt for myelodysplastic syndromes and COTI-2 for triple negative breast cancer, may be more sensitive to the cancers in cluster A1 than in cluster A2.Therefore, our study findings were considered to be of great significance in the context of expanding personalized precision medicine based on the information of genetic mutations, including TP53 genotype, through the introduction of cancer gene panel examinations into clinical practice.