A reduction of myeloid cell cholesterol in vitro and in vivo via a targeted, biomimetic approach prior to conditioning with PCa EVs prevented the uptake of PCa EVs by recipient myeloid cells, abolished NF-κB activity, decreased osteoclast differentiation, stabilized thrombospondin-1 expression and led to reduction of metastatic burden by 77% [117]. The gene discussed is NFKB1; the disease is posterior cortical atrophy.