In an in vitro and subcutaneous animal model, Foretinib upregulated the PD-L1 expression in tumor cells through the JAK2-STAT1 pathway while compromising the function of diverse immunosuppressive cells, such as TAMs and MDSCs, simultaneously, hence synergizing with the anti-PD-1 antibody to enhance the T cell anti-tumor response through relieving the immunosuppressive factors within the TME [37]. The gene discussed is STAT1; the disease is neoplasm.