Conversely, loss of the dNTP catabolic activity of SAMHD1 would lead to expansion of dNTP pools, which could be anticipated to alleviate replication stress, consistent with the abundance of literature showing the rescue of replication stress in cultured cancer cells by treatment with exogenous nucleosides or their precursors [132, 133, 134, 135, 136]. Here, SAMHD1 is linked to cancer.