By contrast, NRF2 was found to transcriptionally induce FAO genes and lipases promoting the degradation of damaged lipids [86], a mechanism that might provide reducing power in the form of NADPH also in cancer cells, since CPT1 inhibition by etomoxir in SF188 glioblastoma (GBM) cells was found to markedly deplete the ATP and NADPH levels, inducing ROS accumulation [96]. Here, NFE2L2 is linked to glioblastoma.