This work has been carried out within the framework of a study on SARS-CoV-2 spike glycoprotein furin cleavage site evolution. The polybasic motif (originally PRRA) present at the S1/S2 junction has two arginine codons CGG–CGG, whose usage is rare in coronaviruses. It has no analogy in other “linage B” beta‐coronaviruses, including neither the Laos closest known relatives of virus behind covid. An hypothesis for theprobable PRRA human origin includes recombination between the genome of a SARS-CoV-2 progenitor and mRNA transcripts within human infected cells. At protein level, the furin arginine pair is evolutionarily strictly conserved, however, the CGG–CGG code can be optimized by the virus itself through synonymous base substitutions. Here I show that the GISAID SARS-CoV-2 EE.2 lineage isolates (accessed June 29, 2023), 531 out of 1,021 (52.2%) have already optimized this furin CGG–CGG code. It has changed to CGA–CGG. As a new brand of the lineage all these 531 isolates share the same mutation in the third position of the first of the two arginine codons. In addition of the codon usage bias affecting R682 there are also two non-synonymous base substitutions N679K and P681R. The earliest date of the SARS-CoV-2 EE.2 lineage was September 12, 2022. Based on NCBI Virus database, from this date appear 1,028 different SARS-CoV-2 lineages. The majority was XBB.1.5 (64,232 isolates 17.17%). However, the ranking position of the EE.2 lineage was 167 (331 isolates, 0.088%), still in the first quartile. Results provide insight into the change of an extremely rare genetic footprint that within an exogenous 12-nucleotide fragment that was imprinted in the SARS-CoV-2 S gene.