A non-coding silencer near LMNB1 constrains lamin B1 expression specifically in oligodendrocytes via CTCF‑mediated looping and PRC2 recruitment. Loss of this element—through upstream deletions or tandem duplications—drives overexpression and explains the tissue‑specific pathology of autosomal dominant leukodystrophy (ADLD).

An intragenic viral silencer within the HTLV‑1 provirus recruits the host RUNX complex to dampen sense‑strand transcription and promote latency. Disrupting this element boosts HTLV‑1 expression and immunogenicity; inserting it into HIV‑1 suppresses production—revealing a portable, cis‑acting latency switch.

A dual-function cis-regulatory element (“ESpromoter”) can act as both enhancer and silencer to tune ATP2B4 and LAX1 in human T cells; its allele-specific interaction with rs11240391 helps explain severe malaria risk.