For example, blood-borne C. neoformans can undergo prolonged interactions with the vasculature during invasive cryptococcosis [18] and, according to our above prediction, this prolonged interaction could result in the cryptococcal-induced overexpression of host urokinase, leading to the ‘phenotypic switch’ of endothelial cells from procoagulative to profibrinolytic states and a plasmin-dependent, pro-invasive microenvironment (Fig. 10). Here, PLG is linked to cryptococcosis.