Recent work suggests that RNase H2 subunits and cellular activity (Wilkins et al., 2025), as well as RNase H2 localisation to HO-TRCs (Goehring et al., 2024), might be responsive to RS produced by the chemotherapeutic agents CPT and HU, and RNASEH2A overexpression in prostate cancer cells can attenuate CPT-induced apoptosis (Kimura et al., 2022). The gene discussed is RNASEH2A; the disease is Familial prostate cancer.