Consistent with recently reported primary familial brain calcification (PFBC) NAA60 frameshift variants associated with NAA60 truncation and destabilization, the frameshifting 2 bp deletion (Asp40Leu) introduced in our NAA60 KO HAP1 clones similarly leads to a significant truncation in the NAA60 protein, resulting in the deletion of the GNAT domain and rational loss-of-function, as demonstrated by in vitro NAT activity profiling of similarly truncated NAA60 variants [20]. The gene discussed is HAP1; the disease is bilateral striopallidodentate calcinosis.