HIF1A

So defective anaplerosis into the mitochondrial chain.

And even in MMA, there was a study showing defective mitochondrial clearance, which So this mitochondrial stress could elevate markers, you know, such as ROS, which would feed into pathways like NF-kappa-B, HIF-1-alpha, and then amplify this inflammatory response.

Then there are some pathways that are maybe even further from the patient, such as the actual short-chain fatty acids binding to HIF.

cell surface receptors like GPR41 and 43, and also altered interferon signaling has been discussed in some patients, but that's more acting as sort of testable mechanism rather than any established explanation at the moment.