RNASE1 and cancer: This suggests that ZAKα could be a potential target for therapeutics aimed at modulating the effects of RNase L. This is especially relevant since RNases are already being used or tested for cancer therapy, such as RNase A.66,67 We speculate that a component of the mechanism behind these RNase therapies could result from ZAKα activation via ribosome stalling and/or collisions that occur as a result of RNase activity in the cytoplasm.