In both cases, infection by pathogens leads to activation of toll-like receptors (TLR), triggering intracellular signaling cascades of the inflammatory transcription factors Relish, Dorsal, and Dif, homologous to NF-κβ, and signaling pathways as JAK/STAT and JNK [4, 33, 72]. The gene discussed is SOAT1; the disease is infection.