This is becoming increasingly important for NfL-based investigations of normal aging (Khalil et al., 2020), as well as cerebrovascular disease (Gattringer et al., 2017; Duering et al., 2018; Tiedt et al., 2018; Peters et al., 2020), atrial fibrillation (AF) (Polymeris et al., 2020), and dementia (Zhao et al., 2019), where accumulating age-related comorbidities might both interfere with the homeostasis of NfL and directly induce neuronal damage per se (Barro et al., 2020; Gafson et al., 2020). This evidence concerns the gene NEFL and cerebrovascular disorder.