To investigate whether HSV-1 modulates FASN during infection, we conducted experiments using SH-SY5Y neuron-like cells, a suitable in vitro model for HSV-1-associated neurological disorders [14], under fully confluent and serum-free conditions, which allowed us to determine whether the observed lipid production is de novo rather than derived from external nutrient uptake. The gene discussed is FASN; the disease is nervous system disorder.