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ATP-sensitive potassium gain-of-function mutations and mutations in the mitochondrial asparaginyl-tRNA synthetase 2 gene can manifest as developmental delay, epilepsy, and neonatal diabetes syndrome (87, 88)
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They intensify T17-cell-mediated inflammation via the G protein receptor (GPR183), leading to aggravated skin conditions in the IMQ-triggered mouse model of psoriasis (68)
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Moreover, gene-environment interactions, often mediated by epigenetic modifications, may further modulate susceptibility to carcinogenic effects of NSW, complicating causal inference 11
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