Evidence suggests that UCN stimulates kinase phosphorylation, promoting breast cancer proliferation.[49] UCN1 has been observed to enhance the expression of ICAM1 through 2 distinct pathways: the cPLA2-NF-κB pathway and the cPLA2-COX2-PGE2-PKA-CREB pathway.[50] ICAM1 mediates the interaction between cancer cells and T-cells, which is pivotal in forming a T-cell deficient TME. This evidence concerns the gene CREB1 and breast carcinoma.