It is worth noting that claudin-3 (CLDN3) and claudin-4 (CLDN4) have been reported to be implicated in dictating malignant progression in prostate cancer, especially in neuroendocrine tumors similar to CDRs.29, 30, 31 However, no significant correlations between CDRs or E2F1 and CLDN3/CLDN4 expression were observed (Fig. S7A, B), and CDRs depletion did not statistically affect CLDN3 or CLDN4 expression (Fig. S7C), indicating that CDRs and CLDN3/CLDN4 likely promote tumor progression through distinct molecular pathways. This evidence concerns the gene CLDN3 and neuroendocrine neoplasm.