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Human genetic support can raise confidence in drug targets for specific indications before investing in clinical trials. De-risking a target this way lowers the bar for chasing novel biology, rather than everyone crowding around the same validated targets and competing purely on chemistry. This space is often criticized for its paucity of successful examples, and a stubborn reliance on PCSK9 as proof of concept, a case that may not generalize to other biology. Part of the problem is timing. Target discovery to approval typically takes 10-20 years, and sufficiently powered GWAS studies have only existed since around 2010. That combination means we still have a limited list of examples where human genetics acted as a genuine catalyst, accelerating the development of a specific asset rather than validating it retrospectively. Still, the few success stories are worth highlighting as they can raise awareness that the concept is generalizable beyond lipid biology, and can serve as case studies for picking future targets. In this post, I trace the story of TYK2 inhibition, a target strongly supported by human genetic data across multiple autoimmune diseases, which has already delivered an approved drug for plaque psoriasis and psoriatic arthritis.