This atypical expression of nuclear vimentin has been reported as a cell survival mechanism via ATM kinase that phosphorylates vimentin in response to DNA damage on colorectal and lung cancer cells HCT-116 and A549, respectively, triggering EMT to increase cell motility and metastatic potential on early stages of treatment with the traditional chemotherapeutic drug camptothecin [58]. Here, VIM is linked to lung carcinoma.