AKR1C1 and non-small cell lung carcinoma: Shi et al. (2019) found that high expression of YTHDF1 is associated with better hypoxic adaptation suppression of non-small cell lung cancer (NSCLC), however when its depletion causes cancer cells to develop resistance to cisplatin (DDP) therapy via the KEAP1-NRF2-AKR1C1 axis, especially the accumulation of reactive oxygen species (ROS) induced by cisplatin treatment. Also, By stabilizing MAP2K4 and MAP4K4mRNA transcription, YTHDF2 activates MAPK and NF-κB signaling pathways promotes the expression of pro-inflammatory cytokines, and aggravates the inflammatory response (Yu et al., 2019).