Previous studies had reported that the adhesion of cancer cells to fibronectin facilitated carcinogenesis and induced resistance to chemotherapeutic agents.[25] In the heterospheroids, the administration of the BRAF inhibitor increased fibroblast activation and induced the formation of tumor stromal niche, whereas, in the monospheroids, no fibronectin formation was observed regardless of treatment with vemurafenib (Figure 3Div). The gene discussed is BRAF; the disease is neoplasm.