By disrupting p53’s binding to DNA and the activation of genes such as CDKN1A, BAX, and GADD45, these mutations contribute to uncontrolled cell proliferation, the evasion of apoptosis, genomic instability, and, in some cases (e.g., R175H and R248Q), more aggressive tumor phenotypes, increased metastatic potential, and chemotherapy resistance [9,45,46]. Here, TP53 is linked to neoplasm.