JUN, as a kernel factor of the AP-1 family, promotes the invasion of tumor cells by activating Matrix Metalloproteinases and at the same time down-regulates the expression of MHC-I class molecules to evade the recognition of cytotoxic T cells; the secretion of IL-6/IL-8 induced by it can also recruit immunosuppressive myeloid cells and inhibit T cell function (62–64). Here, JUN is linked to neoplasm.