Epstein–Barr virus genes activate oncogenes such as Bcl-2 and MYC, as well as signaling pathways such as NF-κB, JNK, JAK/STAT, and PI3K/Akt, and inhibit tumor suppressor DOK1, PKR, p53, PRDM1, DICE1, PTEN, and p27kip1, p21WAF1/CIP1, p16INK4A, p73, etc. The time from viral infection to tumorigenesis is usually shorter in EBV-associated neoplasms with specific oncogene activation. The gene discussed is SOAT1; the disease is neoplasm.