MED23, a key component of the tail modules of the mediator complex, exerts distinct functions in various biological processes, such as hematopoietic stem cell differentiation, carcinogenesis, and angiogenesis.[73, 74, 75] It's noteworthy that our previous research has displayed that Med23 deletion significantly increases the effector function of conventional T cells, thereby repressing tumor development in PyMT model, in which the expression of middle T oncogene in mammary epithelium is prior to the full establishment of TRM cells. Here, MED23 is linked to neoplasm.