CAFs were previously reported in several studies to drive an immunosuppressive microenvironment in tumours by affecting the reprogramming of tumour-associated macrophages to an M2-like phenotype via secretion of Chi3L19, restricting the accumulation of T cells in tumours56,57, modulating T cell immunity towards Th1 function58, and by direct antigen-dependent killing of CD8+ T cells59. The gene discussed is CD8A; the disease is neoplasm.