It is speculated that Hp infection may lead to the increase of ApoB/ApoA1 by causing the occurrence and development of inflammation in the host, and the increase of ApoB/ApoA1 is involved in the interaction between Hp and host cells, and mediates the further progress of inflammation, ultimately leading to atherosclerosis and increased risk of cardiovascular and cerebrovascular diseases. The gene discussed is HP; the disease is atherosclerosis.