rILYd4 was shown to enhance complement‐dependent cytotoxicity (CDC) in rituximab resistant lymphoma cells and a mouse model system.[21] Similar strategies showed promise for inhibiting the enveloped virus HIV‐1, which cloaks itself in CD59 during virus budding.[22] Whilst none of these strategies have led to a clinically approved drug targeting CD59, the results underscore the potential of CD59 as a therapeutic target. The gene discussed is CD59; the disease is lymphoma.