Although most key mutations of acute leukemia like Fms-related tyrosine kinase 3 internal tandem duplication (FLT3-ITD) and nuclear pore protein 98-nuclear receptor-binding SET domain protein 1 fusion gene (NUP98-NSD1) were found to be reserved in PDXs[42], the SVAFs of some key mutations like nucleophosmin 1 (NPM1), tumor protein p53 (TP53), and isocitrate dehydrogenase 2 (IDH2) showed greater divergence in PT-PDX pairs[30], partly due to their roles at later stages of leukemogenesis and the mice-specific pressure on genetic evolution[43]. The gene discussed is TP53; the disease is acute leukemia.