KYAT1, also known as kynurenine aminotransferase 1 or CCBL1, is a bi-functional enzyme that plays a major role in Se-methylselenocysteine (MSC) metabolism. It can catalyze transamination and beta-elimination activities with MSC as a substrate, producing methylselenol (CH3SeH), a cytotoxic selenium metabolite causing apoptosis in cancer cells [3]. It is also involved in the kynurenine pathway, which is associated with the production of neuroactive metabolites like kynurenic acid [5].

In the context of disease, KYAT1 has been implicated in several conditions. In Prader-Willi syndrome, its differential expression was observed in liver steatosis, with levels increasing from grade 1 to grade 3, suggesting its potential as a biomarker for detecting this condition [1]. In rats exposed to a heavy-metal mixture, altered levels of KYAT1 were associated with neurological impairments, hypothesizing a link between the dysregulation of ferroptosis and kynurenine pathways and neurological damage [2]. In critically ill patients, KYAT1 mRNA expression in skeletal muscle was reduced, and this lower expression was associated with a lower risk of weakness. Therapeutic interventions like withholding parenteral nutrition in the first ICU week led to higher KYAT1 expression [4]. In COVID-19 patients with ARDS, KYAT1 was among the proteins with high variable importance in a random forest model for COVID-19 [7]. In pink-eyed white mink, KYAT1 was suggested as a possible gene related to body weight [6].

In conclusion, KYAT1 is an enzyme with key functions in metabolism and is associated with multiple disease-related processes. Its involvement in liver steatosis in Prader-Willi syndrome, neurological impairments in heavy-metal-exposed rats, critical illness in humans, and body weight in mink highlights its significance in understanding these biological and disease conditions. The study of KYAT1 in these contexts provides insights into potential biomarker discovery and disease mechanisms [1,2,4,6,7].