In malignancy cell models, MYC proteins are usually overexpressed, favoring formation of MYC/MAX dimeric complexes, which promote transcription, leading to cell hyperproliferation, and thereby inducing tumorigenesis [89]; however, in the presence of MIZ1, tumor-favoring conditions are restored to equilibrium, as MIZ1 forms a ternary complex with MYC/MAX, which represses MYC-activated genes and suppresses hyperproliferation [90]. The gene discussed is MAX; the disease is neoplasm.