In BC, certain mutations in the tumor suppressor gene p53 have been shown to lead to protein misfolding and accumulation within cells.[12] The normal p53 protein plays a pivotal role in maintaining genomic stability, regulating the cell cycle, and inducing apoptosis.[13] When p53 loses its functional integrity due to mutation and forms aggregates, it not only forfeits its tumor-suppressive capabilities but might also trigger the aggregation of additional proteins, thereby promoting carcinogenesis. This evidence concerns the gene TP53 and neoplasm.