A particularly promising candidate is sunitinib, a receptor tyrosine kinase (RTK) inhibitor targeting VEGFR, PDGFR, c-KIT, and Flt-3; in preclinical models, sunitinib decreased tumor microenvironment (TME) accumulation of myeloid-derived suppressor cells (MDSCs), restored Th1/CTL functionality, muted PD-L1 expression on tumor-resident DCs, depleted CTLA-4/PD-1 expression on activated CTLs, and inhibited production of inhibitory IL-10, TGF-β, and FoxP3 from TILs (58, 59). The gene discussed is CTLA4; the disease is neoplasm.