In contrast to tunicamycin‐induced and PERK‐mediated translation attenuation which is entirely driven by the ISR, we found that the decrease in protein synthesis following HF treatment is ISR‐independent because it is not significantly different in wild‐type cells, GCN2 knockout or eIF2αA/A MEFs and in human cells where GCN2 has been knocked down. This evidence concerns the gene EIF2AK3 and hydrops fetalis.