Previous studies have shown that the PI3K-Akt pathway can regulate HIF1A and further regulate the transcriptional expression of downstream genes.18–20 HIF1A has also been confirmed to be an upstream transcriptional regulator of CXCL12.21,22 We analyzed the expression of tumor-infiltrating fibroblasts in the ST data and found that HIF1A expression was increased in fibroblasts in hypermetabolic regions (Fig. 9d), and there was a significant correlation between HIF1A and CXCL12 expression (Fig. 9e). The gene discussed is HIF1A; the disease is neoplasm.