In resting T cells, increased expression of BTN3A2 was causally associated with decreased risk of asthma (weighted mode causal estimate = −0.056 log odds decrease per s.d. increase in BTN3A2), both childhood- and adult-onset asthma (−0.047 and −0.039, respectively), allergic rhinitis (−0.044), PSC (−0.440), and systemic lupus erythematosus (SLE; −0.256). This evidence concerns the gene BTN3A2 and Adult onset.