The MSI-related P02 tumor originated through alterations in cell cycle, PI3K, and CRG-related pathways (RB1, PTEN, and KMT2B mutations in C1 clonal population), while TP53 mutation occurred specifically in the sarcomatous-related subclonal population C2 (Fig. 4A; Supplementary Fig. S12). This evidence concerns the gene KMT2B and neoplasm.