Many lncRNAs sequester proteins from their targets. (A) NRON sequesters phosphorylated NFAT in the cytoplasm. NRON scaffolds NFAT within a complex that includes the calmodulin-binding protein IQGAP1, the nuclear importer KPNB1, and the inhibitory kinase LRRK2, keeping NFAT in a phosphorylated inactive state. T-cell activation leads to increased Ca2⁺ levels, causing disassembly of this complex and NFAT dephosphorylation, which in turn favors NFAT nuclear import and subsequent activation of cytokine expression. (B) lnc-DC promotes the terminal dendritic maturation gene program. lnc-DC binds the C terminus of STAT3 and sequesters it away from the phosphatase SHP1, preventing its dephosphorylation and favoring nuclear import of phosphorylated STAT3 and subsequent activation of the terminal DC differentiation gene program. (C) PACER promotes COX2 activation in cis. PACER is induced as part of the inflammatory response in response to lipopolysaccharide (LPS) stimulation. PACER binds to and competes with the repressive NF-κB1 homodimer away from the adjacent COX2 promoter, favoring binding of the activating RELA/NF-κB1 heterodimer to the promoter and subsequent COX2 activation. (D) Lethe tunes inflammatory responses in trans. Lethe, a chromatin-retained lncRNA, is transcribed from the Rps15a-ps4 pseudogene and acts as an RNA decoy that titrates activating RELA complexes away from target gene promoters, restraining cytokine activation downstream of inflammatory triggers.