They identify relationships between individual driver genes and certain immune-related features, including enhanced M2 polarization of macrophages in IDH1-mutated BTC (cluster 3) and low immune infiltration in BTC with FGFR2 fusions or rearrangements (cluster 4), providing initial evidence for combining the targeted inhibition of specific drivers to reprogram the tumour immune microenvironment in combination with systemic immunotherapy [95]. The gene discussed is FGFR2; the disease is neoplasm.