Despite the detection of all soluble complement components in the HGSOC microenvironment, our data suggest that tumor cells are spared from complement attack because of the presence of inhibitory receptors and membrane-bound complement regulatory proteins, such as CR1, CD46, CD55, and CD59, which, however, have been shown to not block the protumorigenic effects of complement (86). The gene discussed is CD59; the disease is neoplasm.