However, this observation is inconsistent with our model of the upregulation of let-7g by NGN-attenuated KRAS–PI3K–Rac1–Akt axis metabolic functions, probably because the study cited used a hepatoma cell that conferred the cell-type specificity of miRNA expression to post-translational regulation of the expression of PI3K–Akt-regulated mRNAs involved in metabolism. The gene discussed is RAC1; the disease is hepatocellular carcinoma.