Developmentally, the INSD phenotype, defined in youth as having parent- or self-reported insomnia and sleeping objectively for >7.5 h, has been characterised in five studies by normal cortisol (Fernandez-Mendoza et al., 2014) and C-reactive protein (Fernandez-Mendoza et al., 2017) levels, yet increased beta EEG power during SOL (Fernandez-Mendoza et al., 2016a) and clinically elevated externalising behaviours (Calhoun et al., 2017; Fernandez-Mendoza, Calhoun, et al., 2016). This evidence concerns the gene CRP and insomnia.