Previous studies in our laboratory have shown that SIM2s is a tumor suppressor in breast cells, and we demonstrated that SIM2s suppressive action is in part mediated through the transcriptional repression of EMT factors and the NFkB pathway and that SIM2s promotes DNA damage repair through its direct interactions with ATM and the stabilization of replication forks35,36,43,44,48. Here, ATM is linked to neoplasm.