In BM, a complex TME is formed through the interactions between cancer cells, immune cells, and resident cell types such as astrocytes.[41] Our team previously identified that BM exhibit a unique TME compared to the primary lung cancer.[17] Therefore, we explored the biological functions of radiomic signatures in BM and found that the overall upregulation of IFN response, increased infiltration of CD8+ T cells, and high abundance of CE9 and CE10 are observed in the low‐risk group. The gene discussed is IFNA1; the disease is cancer.