The molecular landscape of ATC is characterised by a high tumour mutational burden, an immunologically ‘hot’ tumour microenvironment with high expression of various inhibitory immune-checkpoint mediators, including PD-L1, and increased neoangiogenesis (VEGFR/FGFR signalling) (6, 31), all of which provide a strong mechanistic rationale for combining ICI with anti-angiogenic agents. This evidence concerns the gene KDR and neoplasm.