In particular, our results support the pre-clinical evidence regarding the candidate role of the circadian pathway as a tumour suppressor circuit acting through the transcriptional control of (or the direct interaction with) key regulators of cell proliferation, apoptosis and DNA repair (and thus genomic stability) and metabolism, such as Ciclin-D1, c-Myc, Mdm2, p53, Gadd45-alpha, Atm, Chk1, Nampt and Sirt-1 [4, 24, 25], which are well known to play a pivotal role in carcinogenesis. Here, CHEK1 is linked to neoplasm.