In addition, various studies have suggested that repression of ISYNA1 (with accompanying reductions in MI generation) could serve as a common mechanism of carcinogenesis across tissues (e.g. 51,52), while on the other hand ectopic ISYNA1 expression increases MI content and suppresses tumour growth [52], which is likely related to ISYNA1 being a direct target of the tumour suppressor p53 [52] and induced by the cell-cycle regulator E2F1 [53]. Here, ISYNA1 is linked to neoplasm.