Interestingly, following intracellular transfection with poly (I:C), which stimulates the RIG-I/MDA5-MAVS pathway, P1’s SV40-fibroblasts clearly had low levels of IFNB, IFNL1, and IFIT1 production, consistently below those of any of the other fibroblasts with TBK1 mutations (G159A/WT or W619*/W619*, from two previously reported patients—one with HSE and the other with systemic autoinflammation (8, 14)—tested here; Fig. 3 B), although the difference between P1’s and other TBK1-mutated SV40-fibroblasts did not reach statistical significance in these experiments. The gene discussed is MAVS; the disease is herpes simplex encephalitis.