In 1994, Smyth et al. reported their experience with the use of botulinum toxin type A for the treatment of bilateral bite hypertrophy, which was considered a revolutionary new approach. Botulinum toxin is a biotoxic more potent polymeric protein neurotoxin produced under anaerobic conditions by Clostridium botulinum of the genus Clostridium. Botulinum toxin is divided into seven types: A, B, C, D, E, F, and G. They have similar chemical structure and pharmacological effects, but different antigenicity. type A botulinum toxin is mainly used to cause muscle atrophy through its chemical denervation or functional denervation after local muscle injection. Botulinum toxin type A selectively acts on the nerve-muscle contacts of peripheral cholinergic motor nerve endings, blocking the efflux of calcium ion-induced acetylcholine vesicles and inhibiting the release of presynaptic acetylcholine, resulting in disuse paralysis and progressive atrophy of muscle tissue. The blocking effect of botulinum toxin type A is considered irreversible. However, because the axons of the nerve endings can continuously “bud” and are accompanied by the continuous renewal of the motor endplates, the nerve-muscle contact points of the nerve endings can create new contact points, which means that the muscle atrophy caused by botulinum toxin type A is reversible. Botulinum toxin has been used in China for more than 10 years, and it is used to atrophy and reduce the size of the bite muscle through the loss of neurotrophic effect, thus achieving the purpose of “slimming the face”. At present, we use Botulinum toxin type A in clinical practice, because it is highly toxic and stable, easy to produce and preserve.