Since USP39 has the ability to modulate pre-mRNA splicing to affect tumor progression, we propose that compared to other USP inhibitors, such as USP7 inhibitors, which inhibit USP7 deubiquitination function by covalently or non-covalently binding to catalytic residues of the catalytic structural domain (97), USP39 inhibitors may inhibit USP39 deubiquitination activity by binding to the reaction site of the non-catalytic structural domain to inhibit the malignant progression of tumors. This evidence concerns the gene USP39 and neoplasm.