In a recent publication from our group, the degradation of NR4A1 using a novel NR4A1 proteolysis targeting chimera (PROTAC) in melanoma models increased tumor-infiltrating B cells, increased CD8+ effector memory cells, decreased monocytic myeloid-derived suppressor cells, and reduced tumor growth and metastasis [26]. The gene discussed is NR4A1; the disease is neoplasm.