TGFB1 and neoplasm: Overall, when coupled with the enhanced proximity of Lepr reporter activity to blood vessels in SCC-CSCs (Extended Data Fig. 7d), our results provide compelling support for a model in which increased angiogenesis at the invasive SCC front endows the tumour microenvironment with an ample supply of leptin, while perivascular-associated immune and other stromal cells6,19 provide the TGFβ necessary to induce Lepr expression in CSCs.