To the best of our knowledge, this study is first to report G2/M arrest induction by SLC22A18 and the mutually inhibitory activity with KRAS. Although inhibition of colony formation, induction of cell cycle arrest and inhibition of xenograft tumor growth were seen from overexpression of SLC22A18 which in itself could have toxic effects, epistatic relationship with KRAS supports that the observed tumor suppressor activities of SLC22A18 is endogenous to the gene. Here, SLC67A1 is linked to neoplasm.