We already contributed to available knowledge by showing that PCa patients display tissue overexpression of PTX3/C1q deposits and of C3a and C5a receptors, inactivation of the terminal complement complex C5b-9, and a significant increase of complement inhibitor CD59, suggesting at least a strong association if not a definite cause–effect relationship between PTX3 tissue overexpression and PCa development, through modulation of complement activation [14]. This evidence concerns the gene CD59 and posterior cortical atrophy.