BCL2L11 and neoplasm: The removal of excessive intracellular ROS prevented the apoptosis of tumor cells and promoted migration and invasion of tumor cells.[54, 55, 56, 57] Surprisingly, on the one hand, the apoptosis pathway (e.g., MYC associated factor X (MAX), myocyte enhancer factor 2C (MEF2C), BCL2 like 11 (BCL2L11), BH3 interacting domain death agonist (BID), caspase 3 (CASP3), and apoptotic peptidase activating factor 1 (APAF1)) was downregulated in DCIS_adjIDC compared with DCIS_Pure (Figure 5I,J).