According to pre-clinical evidence, activation of PARP enzymes in the central nervous system seems to have a role in neuronal death and circadian regulation, which could explain the headache and insomnia observed with PARP inhibitors [63,64], while niraparib interaction with dopamine, noradrenaline and serotine transporters as well as with the dual specificity tyrosine phosphorylation regulated kinase 1A (DYRK1A) receptor could justify the cardiovascular effects of this drug [65]. This evidence concerns the gene PARP1 and insomnia.