However, EGFR TKIs might hijack the key DNA replication/repair components and impair these processes for promoting single tumor cells to acquire multi-level molecular alterations at the genetic, transcriptional, post-translational, and epigenetic levels and ultimately boost intrinsic tumor heterogeneity for genome wide mutation generation (Majem and Remon, 2013). This evidence concerns the gene EGFR and neoplasm.