Interestingly, a similar pattern has been observed in the 5xFAD Alzheimer's disease model, where CARD9 deletion led to increased amyloid‐beta (Aβ) deposition, neuronal loss, cognitive decline, and altered microglial activity.[13] These observations highlight CARD9 as a potential therapeutic target for both T1D‐associated neuropathy and neurodegenerative diseases. This evidence concerns the gene CARD9 and Alzheimer disease.