MYC and neoplasm: The results showed that pathways associated with cell proliferation (MYC targets, G2M checkpoint and oxidative phosphorylation) and protumor pathways (epithelial-mesenchymal transition (EMT) and angiogenesis) were upregulated in the post-treatment samples compared with the pre-treatment samples (Fig. 2A), indicating that surviving tumor cells not killed by NACT may have higher proliferative activities and a greater ability to metastasize.