 0\) [Figure 0](#fig0){ref-type="fig"} convincingly demonstrates that the R00P and K00D mutations in eIF0A destabilize the closed/Pin conformation of the 00S PIC at UUG codons in vitro. Could they extend these results by showing a decreased UUG/AUG start codon usage in a cell-free translation system from eIF0A-mutant cells as compared to wildtype?  