LCP2 (lymphocyte cytosolic protein 2) is an adapter protein critical for T-cell receptor (TCR) signaling and immune cell activation. Upon phosphorylation by ZAP70 kinase, LCP2 mediates interactions with VAV1, NCK, and ITK, subsequently activating PKC-theta and NF-κB transcriptional activity in response to TCR and CD28 costimulation 1. Beyond T cells, LCP2 functions in platelets, mast cells, and NK cells, playing essential roles in AGER-induced signaling that activates p38 MAPK and ERK1/2, promoting pro-inflammatory cytokine release 2. Base-editing screens identified LCP2 as harboring critical residues that tune T-cell activation and cytotoxic function, revealing both gain-of-function and loss-of-function alleles 3. Pharmacological modulation through antisense oligonucleotides suppresses TCR-mediated T-cell activation and FcεR1-mediated mast cell activation, offering potential therapeutic approaches for autoimmune diseases 4. Clinically, LCP2 upregulation correlates with enhanced CD8+ T-cell infiltration and improved survival in metastatic melanoma patients receiving anti-PD1 immunotherapy 5. In diabetic retinopathy, LCP2 inhibition reduces T-cell apoptosis and oxidative stress via PD-1/PD-L1 pathway modulation 6. Additionally, LCP2 serves as a potential biomarker of microglial activation in humans 7 and is implicated in preeclampsia pathogenesis as a hub gene in immunity-related pathways 8.