Since PTEN, WNK2, SOX6, BTG3, and RBSP3 have putative miR-18a-binding sites in their 3′-UTRs (Supplementary Fig. S6a) and act as tumor suppressors in CC [18, 26–28], we hypothesized that miR-18a enhances PD-L1 expression via targeting these candidate targets. Here, CTDSPL is linked to neoplasm.