The need for such studies becomes extremely urgent also on the basis of a very recent study [146] showing that the loss of protein kinase Cλ/ι (PKCλ/ι) promotes HCC by enhancing OXPHOS, in spite of activation of Nrf2—which, according to the literature, is known to redirect metabolism towards glycolysis [146]. This evidence concerns the gene NFE2L2 and hepatocellular carcinoma.