Acute MEKi treatment of VPr tumors resulted in significant immune contexture changes, including decreased myeloid-derived suppressor cell occupancy, increased CD8 infiltration, and major histocompatibility complex-I (MHC-I) expression (Extended Data Fig. 7d–f), features previously reported in response to MEKi in other tumor types and con [48, 49]. The gene discussed is CD8A; the disease is neoplasm.