Interestingly, HIV-1 infection effectively enhanced PQBP1–cGAS complex formation, in stark contrast to HT DNA-treated cells, further supporting the specificity for lentiviral recognition in the cytoplasm to trigger a specific antiviral response, rather than an unwanted response to host-derived DNA possibly leaking from mitochondria or the nucleus (see Figure 2B) [7]. The gene discussed is PQBP1; the disease is HIV-1 infection.