Several AD risk genes (APOE, PLCG2, and TREM2) have been shown to be critical for the development and function of DLAMs in response to lipid overload due to host tissue damage in mouse models of AD and demyelination, and other diseases of lipid-rich tissues, highlighting a potential causal link between regulation of the DLAM response and modulation of AD risk8,13–15. The gene discussed is TREM2; the disease is Alzheimer disease.