EIF2AK4 and hydrops fetalis: While ZAK and ribosome stalling/collisions are suggested to be largely dispensable for activation of GCN2 in response to HF treatment, it does not preclude the idea that ribosome stalling/collisions can be an enhancer or perhaps a redundant activator of GCN2 in conjunction with HF activation by direct GCN2 binding with uncharged tRNAs.