Abstract: Set was firstly described as a part of the set-can fusion gene associated with acute undifferentiated leukemia in 1992. The Set protein (SET) expressed widely in human tissues is a multifunctional protein in regulating DNA replication, nucleosome assembly, histone modification, gene transcription and cell apoptosis. It participates in the regulation of testosterone biosynthesis by inhibiting PP2A activity and further activating the lyase activity of P450c17 in those steroidogenetic cells in gonadal system and adrenal gland. Phosphorylation of ser causes cytoplasmic detention of SET which aggravates the protein-protein interaction and then triggers Alzheimer′s disease（AD） pathogenesis and oncogenesis. The SET-binding proteins refer to many major functional groups like metabolism, signal transduction, transcription and translation. Study on the SET-binding proteins revealed new SET functions. Many kinds of bioactive tumor suppressors inhibit SET activation by binding PP2A and activating PP2A function. SET suppressor could be a beneficial approach to prevent cancer growth and metastasis, including prostate cancer, lung cancer and so on. This review will focus on the structure, phosphorylation regulation, regulatory proteins and binding proteins of SET, and summarize the potential antineoplastic drugs targeted on SET.

Key words: Oxidative phosphorylation, Drug interactions, Tumor markers, biological, SET