Increased occurrence of MondoA deficiency in several tumors, including lymphomas, sarcomas, bladder, and colon carcinomas24,64–67, in parallel to the suppression of MondoA recruitment at the Txnip or Arrdc4 promoter upon various oncogenic drivers (Ras, BRAF, PI3K and mTOR) suggests that MondoA silencing may contribute to the transformed phenotype across broad cancer types64,68,69. The gene discussed is BRAF; the disease is lymphoma.