Based on our current understanding, the working model is that MBOAT7 deficiency (either via rs641738-driven or obesity-related suppression) can promote steatosis via 1) activation of the SCAP-SREBP-1c pathway to promote canonical de novo lipogenesis, 2) activation of a noncanonical pathway of lipid synthesis via upregulation of CDS2, or 3) the fatty acid transporter FATP1 is overexpressed facilitating lipid deposition (Fig. 3). This evidence concerns the gene SLC27A1 and steatosis.