This results in decreased MDSC accumulation and a less tumor-favorable microenvironment, highlighting CUL4B’s role in suppressing MDSC function and tumor growth The CRL4B/PRC2/HDAC complex promotes H3/H4 deacetylation, H3K27 trimethylation, and H2AK119 monoubiquitination, disrupting the AKT/GSK3β/β-catenin signaling cascade by inhibiting AKT-specific phosphatases (PP2A and PHLPP1/2). Here, CUL4B is linked to neoplasm.