Given that the efficacy of the parent compound, amiodarone, relies on Myc degradation ​10, and considering Myc’s critical role in regulating cell proliferation​, sensitizing cells to antimitotic agents24–26, and influencing microtubule nucleation and organization ​24–26, as well as the ability of microtubule-targeting drugs to impact Myc activity​57–59, we investigated whether the cancer-specific antimitotic effects of DL78 were driven by Myc modulation. The gene discussed is MYC; the disease is cancer.