After the discovery that HINT1 binds to and inhibits the activity of microphthalmia transcription factor (MITF) provided the first evidence for an additional role of HINT1 in transcriptional regulation11, several transcription factors, including CDK7, AP1, JNK2, USF2, and β-catenin, which can act as oncogenes in several cancer cell types, were also reported to interact with HINT1 and become inactivated6,12–14; this further supports the claim that HINT1 may serve as a tumor suppressor via regulation of gene expression. The gene discussed is MITF; the disease is cancer.