Aberrant, unscheduled SCYP3 expression outside the meiotic context has been shown in other cancers (Chung et al., 2013; Cho et al., 2014a; Kitano et al., 2017), where it has the potential to disrupt the activity of BRCA2, potentially leading to the modulation of strand invasion capabilities for recombinases (RAD51 and DMC1), which in turn drive homologous recombination (Hosoya et al., 2011; Kobayashi et al., 2017) (see above). Here, RAD51 is linked to cancer.