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). The gene discussed is CDS2; the disease is obesity disorder.