Supporting these assumptions is, for example, the direct TGFβ-signalling occurring between platelets and cancer cells, inducing EMT and favouring metastization [43], the turning on or off of demethylases by different melanoma cell clones, giving rise to a mixture of cells with different tumour growth efficiencies [44], or the co-existence of epithelial, mesenchymal and hybrid cancer cell states in lung adenocarcinoma, providing these tumours with increased survival [39]. The gene discussed is TGFB1; the disease is melanoma.