CK2α inhibits the DNA-binding activity of MAX-MAX homodimers but not MYC-MAX heterodimers.23 CK2/CSNK2A1 is involved in cancer progression by phosphorylating various signaling molecules.9 We therefore hypothesized that the switch of MAX-MAX homodimerization to MYC-MAX or β-catenin-MAX heterodimerization may regulate HMGB1 promoter activity through the E-box. Here, HMGB1 is linked to cancer.