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Mutations in critical transporter and enzyme genes disrupt these steps and underlie a spectrum of neurological disorders collectively termed riboflavin-responsive neurometabolic diseases. A representative example is riboflavin transporter deficiency (RTD), caused by loss-of-function mutations in SLC52A2 and SLC52A3 , which encode the riboflavin transporters RFVT2 and RFVT3, respectively

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Table 4 shows, for each mental condition, the top 20 words, ordered by their average importance score, identified by the explainability analysis

Subsequently, Mahimainathans group identified and validated for the first time a series of miRNAs, miR-153, miR27a, miR142-5p, and also miR-144 in neuronal cells, specifically in human SH-SY5Y neuroblastoma cells, which directly mediate repression of NFE2L2 in a KEAP1-independent manner [224]