We confirmed the role of GNPTAB in EBOV infection in both HAP1 cells and primary fibroblasts from individuals with mucolipidosis, a genetic disorder associated with mutations in GNPTAB. While GNPTAB is required for the correct localization of numerous lysosomal hydrolases, and we cannot exclude the involvement of other factors, lack of EBOV infection correlated with the loss of CatB activity, which is known to be required for EBOV entry. Here, GNPTAB is linked to mucolipidosis.