LEPR signalling during SCC progression appears to be rooted in two events: first, a CSC-mediated influx of vasculature within the tumour microenvironment that increases blood vessel density at the invasive front and in turn causes local leptin levels to rise within the tumour stroma; and second, a corresponding rise in perivascular TGFβ that enhances TGFβ signalling and Lepr gene expression within neighbouring SCC-CSCs. Here, LEP is linked to neoplasm.