Indeed, while TLR activation was initially solely considered to bridge innate and adaptive immunity, it is now clear that TLR can also directly affect CD4 T-cell responses.59 60 Importantly, synthetic CDNs, nanoparticulate STING agonists, as well as small-molecule STING inhibitors have recently been shown to exhibit functional activities in vivo.61–63 Our findings could thus be therapeutically exploited to manipulate CD4 T-cell responses in infections, inflammatory diseases, and cancers. The gene discussed is CD4; the disease is infection.