Four of the authors of  “The Origins of SARS-CoV-2: A Critical Review”,  also wrote “Proximal Origin of SARS-COV-2”.   One of their conclusions in this new 2021 article is,  

"This demonstrates beyond reasonable doubt that RaTG13 is not the progenitor of SARS-CoV-2, with or without laboratory manipulation or experimental mutagenesis."    

This conclusion is spurious at best.  They base their conclusion on their analysis of the 1AB gene, disregarding the rest of the genome.  But, RaTG13  1AB gene is 96% identity similar to Covid-19 1AB gene, according to Zhou below. Slightly less than RmYN02, RpYN06 and PrC31's, but pretty close. More importantly,   RaTG13 S gene is 96% identity amino acid similar with Covid-19.  RmYN02, RpYN06 and PrC31  S genes are only 76% and 63% similar to Covid-19, and their RBDs even less.  Making them less likely Covid-19 immediate progenitor.   The better science is represented by the articles,  

"A Novel Bat Coronavirus Closely Related to SARS-CoV-2 Contains Natural Insertions at the S1/S2 Cleavage Site of the Spike Protein", Hong Zhou, Xing Chen, and others  

"Evidence for SARS-CoV-2 related coronaviruses circulating in bats and pangolins in Southeast Asia", by Supaporn Wacharapluesadee, Chee Wah Tan, and others  

"Identification of novel bat coronaviruses sheds light on the evolutionary origins of SARS-CoV-2 and related viruses", by Hong Zhou, Jingkai Ji, and  others

Zhou stated,  

"Phylogenetic analysis of full-length genome sequences of representative sarbecoviruses revealed that SARS-CoV-2 (Covid-19) was most closely related to RaTG13, while RmYN02 and the Thailand strains formed a slightly more divergent clade."            
                                                                                                                          
That is a scientific fact.  Full-length genome analysis points at RaTG13.  No one can defacto say that a RaTG13 related type bat, from 50 years ago, may not be the possible immediate progenitor of Covid-19.  That is bad science.   The authors' second conclusion,
                                                                                
"the claim that the virus was already highly adapted to the human host, or somehow optimized for binding to human ACE2, is without validity"      
                                                                            
Again is a conclusion, that does not take into account the high genomic homology of 99.98%, of many of the first Covid-19 victims.  Most first victims were all hit by the same highly toxic Covid-19 environment at the Hunan Seafood market.  Few mutations, small time period to last ancestor, Covid-19 was ready to go at the beginning of the outbreak.    
                                                                                                                                                                                                  
And the lack of identifiable immediate precursor coronaviruses, point at already highly adapted, not recently evolving from known precursor coronaviruses.  Its divergence date says it had been in nature for at least 50 years already.  Yes, already highly adapted.  The binding affinity of 20% greater than related betacoronaviruses.  More residues to bind human ACE2 in the Covid-19 RBD, leading to more  van der Wals contacts,  according to “Structural and Functional Basis of SARS-CoV-2 Entry by Using Human ACE2”, by Qihui Wang and others. Greater binding affinity.  This says something about Covid-19’s   “optimization”.  Three O-glycans surrounding the furin cleavage site, to help Covid-19 run under the radar of human immune system detection. Not slightly "optimized", but fully locked and loaded.  The 21 scientists all full of logical arguments and plausible scenarios, but short on good science.

Peter G.