Among them, CCL5 and CXCL9 have been widely investigated because their overexpressed levels were correlated with CD8+ T cell infiltration in cancers, namely immunoreactive tumors (30), which supported our results that abundant immune infiltration was enriched in Cluster C. Moreover, targeting CCL5 to augment TGFβ signaling, which was inhibited in Cluster C, is an alternative treatment protocol (31). The gene discussed is TGFB1; the disease is cancer.