ACAT1 and cancer: Some of these metabolic aspects are: 1) the increase in TAG levels, which leads to an increase of DGAT activity (parasitic protozoans), de novo FA synthesis, (e.g., SREBP upregulation in HCV and DENV/ZIKV replication and cancer cells), and increase in FA uptake (cancer cells), and 2) the free cholesterol/SE balance, which is modulated by SREBP (cancer) or aspartyl-like peptidase (e.g., T. cruzi) and the enzyme ACAT, which might display a key role in the parasite’s survival (e.g., T. gondii).