Importantly, the interaction between HDAC6 and TRIM56 was significantly upregulated at 4 h p.i. (Fig. 8D), suggesting that HSV-1 early infection promotes the nuclear-to-cytoplasmic transport of HDAC6 and enhances its interaction with TRIM56, thereby reducing TRIM56-mediated cGAS-STING activation. The gene discussed is STING1; the disease is infection.