The primary importance of the VLDL particle per se in determining its function and fate is emphasised by the recent observation that cardiac VLDL-R is downregulated in sepsis/endotoxinaemia [80]—hence, alterations in VLDL composition are essential determinants in its utilisation, irrespective of specific uptake route (indeed “endotoxic” VLDL secreted during sepsis has been suggested as a vital component of the host immune response [81, 82]). Here, VLDLR is linked to Sepsis.