In many cancers,dysregulation of the MYC/MAX/MXD transcriptionalnetwork leads to an imbalance favoring MYC-MAX heterodimers, whichdrive uncontrolled cell proliferation and repress differentiation.Although MAX itself is not typically overexpressed or mutated, itsobligatory role as a dimerization partner makes it a critical enablerof MYC-driven oncogenesis., MAX is expressed ubiquitouslyand forms stable bHLHLZ-mediated dimers with MYC, enabling bindingto E-box DNA sequences and transcriptional activation of target genesinvolved in cell growth, metabolism and survival., The gene discussed is MAX; the disease is cancer.