(75) reported that treatment-resistant residual tumor cells in organoids, xenografts, and cancer patients entered a dormant diapause-like adaptation to reduce apoptosis priming by suppressing MYC activity or inhibiting MYC transcriptional co-activator BRD4, which could weaken drug cytotoxicity and induce the tumor to be resistant to treatment. This evidence concerns the gene BRD4 and neoplasm.