Collectively, these findings not only provide the first evidence that AKR1C1 is acetylated, but also reveal that the acetylation is an important regulatory mechanism underlying the pro-metastatic potential of AKR1C1, and SIRT2-mediated deacetylation may represent a novel therapeutic strategy for NSCLC patients harboring high level of AKR1C1. The gene discussed is AKR1C1; the disease is non-small cell lung carcinoma.