ACAT1 and neoplasm: In order to test whether this excess of cholesterol is important for tumor formation, we then decided to downregulate the expression of genes involved in cholesterol uptake (LRP1, LpR2) (Figure 2E–H and I–L, respectively) [38], intracellular trafficking (Npc1a) (Figure 2M–P) [39,40], and storage (Figure 2Q–T) (CG8112—ortholog of SOAT1/ACAT1) [41] in a clone-specific manner.