CD4 and neoplasm: The comprehensive monitoring of tumour-reactive CD4+ T cells is hampered by several hurdles, such as tumour antigen selection, HLA class II polymorphism, low frequencies of antigen-specific CD4+ T cells and the plasticity of CD4+ helper T cells.17 One approach to circumventing these obstacles involves the ability of CD4+ T cells to recognise degenerate HLA class II-restricted epitopes from relevant shared tumour-associated antigens.18–21