Genetic knockdown of the E3 ubiquitin ligase, UBR5, in preclinical models of cancer, has shown promise in attenuating tumor growth and enhancing anti-tumor immune response through mechanisms including increased antigen processing and presentation, elevated T-cell infiltration, reduced TAMs recruitment, and reduced PDL-1-mediated immune evasion [30,36,37]. This evidence concerns the gene CD274 and neoplasm.