Chen et al[3] (2023) demonstrated that risk factors such as smoking and hypertension promoted IPN neogenesis by up-regulating the levels of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) in the plaques and stimulating the expression of vascular endothelial growth factor, and the incidence of cerebral infarction in patients with SMI flow score ≥ 2 was 3.2 times higher than that of patients with a low score (P < .05), directly confirming that IPN is associated with inflammation, and that IPN formation is a major cause of inflammatory cell infiltration. This evidence concerns the gene TNF and cerebral infarction.