The origin of SARS-CoV-2 lies in the gain-of-function related to the PRRA spike glycoprotein polybasic furin cleavage site (FCS). The CGG-CGG arginine pair code is unique and rare in the virus. However, novel viruses found in Laos can be considered SARS-CoV-2 ancestors, but they do not have the PRRA. At this point, I have described: (i) the 100% match between the exogenous S gene fragmentencoding PRRA andhuman mRNA RefSeq transcripts; (ii) the related genes are highly expressed in virustarget tissues; (iii) PRRA arginine codon usage bias; (iv) PRRA-like insertions; and (v) the PRRA human origin hypothesis. The aim of this workis to provide further support tothishypothesis. Based on current SARS-CoV-2 sequences (January-March, 2023), here I show that 43 out of 10,644 (0.42 %) GISAID Africa, Asia, Europe and the USA complete genomes and 613 out of 134,022 (0.45 %) NCBI-Virus spike glycoprotein sequences had the CGG-CGG code optimized. The results are in agreement with those in previous works that reveal a viral FCS arginine codon usage bias. Here I also show new found spike glycoprotein PRRA-like insertions (100% match to human mRNA RefSeq transcripts and related genes virus target tissue specifics). In these PRRA-like insertions the human mRNA transcripts should be the origin of the coding S gene fragments. Human is the host of the involved SARS-CoV-2 specimens. They are human viruses isolated from infected human cells. The origin cannot be genetic material from other viruses. Regarding the mechanism, it would be the most common in viruses evolution: recombination. The evolutionary success of the PRRA-like insertions lies in the respect of the reading frame on S gene translation. Results suggest that PRRA spike glycoprotein insertion in a SARS-CoV- ancestor was not an isolated evolutionary event, but rather common in virus evolution.