LYNX1 is a GPI-anchored prototoxin that modulates nicotinic acetylcholine receptor (nAChR) function through allosteric mechanisms 1. It acts as a concentration-dependent modulator of multiple nAChR subtypes, enhancing desensitization and altering single-channel properties 2. At low micromolar concentrations, LYNX1 acts as a positive allosteric modulator of α7-nAChRs, increasing acetylcholine-evoked currents, while higher concentrations produce inhibition 3. The protein regulates nAChR pentameric assembly and shifts stoichiometry toward lower-sensitivity configurations, preventing excessive excitation-induced neurodegeneration. In the central nervous system, LYNX1 is colocalized with nAChRs in brain regions critical for learning and memory 3. Water-soluble LYNX1 variants enhance synaptic plasticity and long-term potentiation while ameliorating cognitive impairments associated with α7-nAChR dysfunction 3. Beyond the brain, LYNX1 is expressed in lung epithelium where it functions as a negative modulator of nicotinic signaling 4. In lung cancer, LYNX1 expression is decreased compared to normal tissue, and its expression suppresses cancer cell proliferation through α7-nAChR modulation and activation of PKC/IP3, MAP/ERK, p38, and JNK signaling pathways 5. These findings suggest LYNX1 serves as an endogenous regulator of lung cancer growth and represents a potential therapeutic target 4.