AKT1 and neoplasm: On the other hand, the establishment of primary tumours are highly dependent on pro-proliferative and growth-stimulatory signalling pathways, and increased membrane cholesterol concentrations promote this through the formation of lipid rafts.152 Indeed, cholesterol-rich lipid rafts facilitate the accumulation of receptor tyrosine kinases, such as HER2 and IGF-1, to rapidly induce oncogenic signalling including PI3K–AKT.153 In this context, inhibiting cholesterol biosynthesis may be beneficial.