TP53 and neoplasm: (3) As the cell proliferation was upregulated by katanin P60, the point mutations might be amplificated by increased number of genetic material duplication, which elevated the expression of tumor promotive genes such as TP53, MYC, and MET, and these genetic mutations might contribute to the development of chemoresistance and reduce the treatment response as well as survival outcomes in NSCLC patients [22].