We found that editing events played a role in lung adenocarcinomas via changing amino acids, modulating alternative splicing patterns, such as in 5’ UTR of HMOX2, or affecting the expression of genes related to tumor stage and recurrence, such as in 3’ UTRs of CTC1 and GNE. Furthermore, by investigating hyper-edited genes only appeared in metastatic but not primary samples, we discovered genes and pathways that contribute to metastasis development, such as MSH2 and XIAP. This evidence concerns the gene MSH2 and neoplasm.