focused on the molecular characteristics of tumor cells that persist after treatment, using patient-derived breast cancer organoids to find that persistently treated tumor cells can eliminate drug cytotoxicity by a molecular adaptation similar to embryonic diapause, namely consuming protooncogene Myc or inhibiting the bromodomain protein 4 (Brd4), a Myc transcription coactivator, to eliminate drug cytotoxicity, providing a potential therapeutic strategy for chemotherapy-resistant tumor cells (60). This evidence concerns the gene MYC and breast carcinoma.