Recent studies have demonstrated that the expression of Fibroblast Growth Factor Receptor 4 (FGFR4) and CD276 (also known as B7-H3) on tumor cells and within the TME contributes to the suppression of anti-tumor immune responses, especially by inhibiting the activity of both CD4+ and CD8+ T lymphocytes through T cell exhaustion [45]. Here, FGFR4 is linked to neoplasm.