Although we did not find significant general splicing defects among patients with CRBN exon-10 splice variant when compared to those expressing the full-length transcript, we identified upregulated TNFA signaling via NFKB, inflammatory response, and IL-10 signaling pathways in patients with exon-10 splice variant across various data sets—all potentially promoting tumor growth via chronic growth signals. The gene discussed is CRBN; the disease is neoplasm.