GLI1 and esophageal adenocarcinoma: 272). Similarly, imiquimod, a nucleoside analogue of the imidazoquinoline family approved for treatment of BCC (Ref. 273), has been shown to induce a PKA-mediated GLI phosphorylation with consequent reduction in GLI activator levels (Ref. 274). Myristoylated aPKC peptide inhibitor (PSI) inhibits phosphorylation and activation of GLI1 by aPKC-ι/λ in BCC (Ref. 40). Rapamycin inhibits TNF-α-induced and mTOR-S6K1, mediated phosphorylation and activation of GLI1 in oesophageal adenocarcinoma (EAC) cells (Ref. 41).