Upon the viral infection, as well as in response to the entry of endotoxin, such as LPS, the cholesterol tends to inactivate their biological toxicity through the selective interaction.32,42 It is well known that decreased cholesterol level in serum and cells drives the dissociation of SCAP-SREBP-2 complex from INSIGs and subsequently the SCAP-SREBP-2 complex translocates to Golgi.14 The SREBPs was cleaved into N-term and C-term by enzymes including S1P and S2P, and the SREBP-2 N-term translocates to the nucleus and activates transcription of lipid synthesis. The gene discussed is MBTPS2; the disease is viral infectious disease.