Given the upregulation of MYO1F expression in microglia within both murine models of neurodegeneration and tissue from individuals with AD (Gao et al., 2023; Matarin et al., 2015; Mukherjee et al., 2019; Zhang et al., 2013), we examined the subcellular localisation of endogenous MYO1F and its adaptor protein ASAP1 in both primary mouse microglia and human iPSC-derived microglia to assess whether recruitment to podosomes is conserved across different myeloid cell types. This evidence concerns the gene ASAP1 and Alzheimer disease.