Mechanistically, in cholangiocarcinoma, atypical protein kinase C-iota (aPKC-ι) directly phosphorylates specificity protein 1 (Sp1) to up-regulate P-Sp1 that increased SNAIL expression by promoting Sp1 binding to the SNAIL promoter, resulting in EMT changes and immunosuppression [19]. This evidence concerns the gene SP1 and cholangiocarcinoma.