These predicted signals were interpreted in the context of angiogenesis (e.g., PTN–NCL), immunoregulatory programs (e.g., HLA-DRA–associated antigen-presentation machinery), and tumor-progression–related pathways, leading the authors to propose that apCAFs contribute to tumor–stroma crosstalk and may favor immune-excluded (“cold”) microenvironments [94]. This evidence concerns the gene NUCLEOLIN and neoplasm.