Additionally, given that MUC1-C transcriptionally cooperates with NF-κB and MYC to drive PD-L1 expression, silibinin’s known suppression of NF-κB and MYC signaling may further destabilize MUC1-C-driven transcriptional programs, weakening its immunosuppressive influence in the tumor microenvironment [87,93]. Here, NFKB1 is linked to neoplasm.