NAT10 (or human N-acetyltransferase-like protein (hALP); EC 2.3.1.xx) is primarily identified as an activator for up-regulating telomerase activity through stimulation of transcription of hTERT together with histone acetyltransferase activity. This gene also responds to DNA damage, in which the transcriptional activity of the NAT10 promoter may be specifically stimulated, and it thus also serves to enhance cell survival in the presence of genotoxic agents[1]. Additionally, NAT10, that localizes mainly in the nucleolus, can mediate nuclear shape rescue in laminopathic cells via microtubule reorganization (tubulin is a known NAT10 substrate). Down-regulation and mutations of the nuclear-architecture proteins lamin A and C cause misshapen nuclei and altered chromatin organization associated with cancer and laminopathies, including the premature-aging disease Hutchinson-Gilford progeria syndrome (HGPS). Inhibition of NAT10 KAT activity in laminopathic cells reduces microtubule anchorage, thereby releasing an external force on the nuclear envelope, and thus contributes to nuclear shape rescue and global enhancement of cellular fitness[2].