The catabolic phenotypes observed in cancer-associated fibroblasts (CAFs) are driven by multiple cell signaling pathways including loss of caveolin-1 and the activation of HIF-1α and NF-κB signaling, which may serve as metabolic vulnerabilities in the metabolic rewiring of the tumor-CAF network (Pavlides et al., 2009; Bonuccelli et al., 2010; Wilde et al., 2017). Here, HIF1A is linked to neoplasm.