MFSD2A and neoplasm: That might be achieved by adding endogenous compounds (such as FSTL1) that are expressed at insufficient levels only under proatherogenic flow conditions or by targeting therapeutics to endothelium expressing inflammatory markers; VCAM-1 (vascular cell adhesion protein 1)–targeting nanoparticles that interfere with MFSD2a signaling have been used to weaken the blood-tumor barrier and hence improve delivery of chemotherapeutics.114