Lack of TIGIT in Tregs post-teplizumab treatment is an important immune target to consider for future intervention strategies because earlier research linked TIGIT expression in Tregs with direct inhibition of Th1 and Th17 responses (Johnston et al, 2014; Joller et al, 2014), reduction of interferon gamma (IFN-γ) in patients with multiple sclerosis, potentially by suppressing IL-12-induced PI3K-AKT-mTOR signaling cascade responsible for inducing dysfunctional proinflammatory Th1 Treg program (Ouyang et al, 2012; Lucca et al, 2019). The gene discussed is TIGIT; the disease is multiple sclerosis.