The small bHLHZip protein MAX functions at the center of a transcription factor network that governs many aspects of cell behavior, including cell proliferation and tumorigenesis. MAX serves as a cofactor for DNA binding by the various members of this network, which include the MYC family of oncoproteins and a group of putative MYC antagonists that include MNT, MXD1-4 (formerly MAD1, MXI1, MAD3 and MAD4) and MGA. The many heterodimerization partners of MAX raises questions concerning the dynamics of MAX interactions and the functional consequences of the switching of Max partners. Here we review the activities of MAX, its interaction partners, and recent results showing that tissues lacking the MAX-interacting protein MNT are predisposed to tumor formation.