Starting on the left-hand side of the figure we have a grey circle which represents an effector T cell. These cells are part of the immune system and have the potential to kill tumor cells directly. The words hypoxia and necrosis are shown which relate to the fact that the tumour microenvironment tends to be hypoxic, meaning with low oxygen levels, and necrotic, meaning cells may undergo a form of cell death that is unregulated and releases material in an way that the immune system detects as inflammatory. As a result of these processes, a molecule called ATP, shown as a dark orange circle with small spikes in the figure, is released in the tumour at high concentrations. ATP is further metabolised by different enzymes to a molecule called adenosine, depicted as small light orange circles in the figure. Adenosine is an important molecule for our cells as it can be used to make a wide number of other molecules including RNA and DNA. At high extracellular concentrations however it is known to have immunosuppressive properties. In the figure we show that adenosine interacts with a specific receptor on the surface of T cells called A_2A. A direct consequence of this interaction is a suppression of effector T cell functions, including the ability to kill tumor cells. This is depicted in the figure with an arrow pointing to an intact tumor cell with the text showing ‘no effect on tumor cells’. On the right-hand side of the figure we have the same generation of ATP due to hypoxia and necrosis, but this time the molecule EOS-850 (now known as Inupadenant), shown as a green molecule in the figure, interacts with A_2A receptor in a way that does not activate it. Importantly, this prevents adenosine from interacting with A_2A receptor. The result is that the inhibition of T cell activation by adenosine is prevented and T cell functions including the ability to kill tumor cells are restored. This is shown in the figure by a green arrow linking an activated T cell to a tumor cell that is fragmenting with green text that says ‘tumor cell killing’.