This apparent discrepancy may be explained by several factors: (1) posttranslational regulation being the primary mode of interaction between DDX3 and HMGB1 (as evidenced by co-IP), (2) tumor heterogeneity diluting cohort-level transcriptional correlations, and (3) limitations in current databases where matched DDX3/HMGB1 protein expression data remain scarce. Here, HMGB1 is linked to neoplasm.