have been conserved throughout evolution and solely found in the ER which is the primary site for the biosynthesis of TGs. Second, when FIT proteins are overexpressed in either the liver of a mouse of even in cells that have been cultured in vivo, there has been observable buildup of lipid droplets that are rich in triglycerides as an outcome. Third, FIT proteins are not DGATs. DGATs facilitate the biosynthesis of the TGs. FIT proteins strictly aid in the conversion of the TGs (made by DGATs) into lipid droplets. Therefore, knowing the function of these FIT proteins helps us to make sense of why they are placed downstream of the DGATs. Lastly, a shRNA-facilitated reduction in FITM2 in adipocytes (3T3-L1) or even a knockdown of it in the embryos of zebrafish resulted in great declines in lipid droplet build-up. FITM2 has been identified as being overexpressed throughout the time 3T3-L1 (from the adipocyte cell line) is being differentiated which shows resemblance to the peroxisome proliferator-activated receptor gamma (PPAR γ) at a specific period when lipid droplets have been identified to build-up which results in the adipocyte phenotype that is seen in the 3T3-L1 cells. The overexpression of FITM2 was also displayed when the 3T3-L1 cells were combined with rosiglitazone (a PPAR γ agonist). This serves as evidence for the idea FITM2 is functionally regulated by PPAR γ. The specificity of the tissue dispersal of FITM1 and FITM2 and the fact that FITM2 binds TG more intensely than FITM1 (which forms a weak bond) presents separate functions for these FIT family proteins in regards to the metabolism of lipids. Lipid droplet development induced by FITM2 may function in TG storage for long-term purposes in adipose whereas FITM1 may function to make the smaller lipid droplets that are seen in skeletal muscle where there is a fast replacement of LDs. Clinical Uses When physiological circumstances are regular, lipid droplets are depended on to keep energy balanced at not only at the cellular level, but for the sake of the whole organism’s sustainability. However, excessive acquirement of lipid droplets can result in obesity, and increased risk for obtaining disease including type 2 diabetes, atherosclerosis, and heart disease. The documentation of the FIT proteins should help in evolving substances to revert FIT expression or activity back to a normal regulatory state as treatment for these diseases. In addition, a recent study was performed on