It is known that phosphorylation of MAX inhibits the DNA-binding activity of MAX homodimers but not C-MYC/MAX heterodimers.24,28 Since we found that CSNK2A1 phosphorylates MAX, we believe this may cause suppression of MAX-MAX homodimer and increase in MAX-C-MYC or MAX-β-catenin heterodimers and further upregulate HMGB1 and IL-6, favoring CCA progression. Here, CSNK2A1 is linked to cholangiocarcinoma.