Together, these findings indicated that FAP+ CAFs that express FGF-2 are present in the B16-F10 tumour stroma and that nintedanib efficiently blocks the proliferation and activation of these cells, with these effects possibly leading to attenuation of the immunosuppression exerted by the TME and an increase in the infiltration and activation of CD8+ TILs. The gene discussed is CD8A; the disease is neoplasm.