This notion is highly supported by our findings that αTAT1 downregulation is both temporally and spatially identical to α-tubulin acetylation changes downstream of MAG or CSPGs treatment (Figs. 3, 4), and that αTAT1 reconstitution by lentiviral-αTAT1 infection can overcome neurite growth inhibition (Fig. 5C,D). This evidence concerns the gene ATAT1 and infection.