It's important to know whether or not the authors picked BsaI & BmBI blind, before looking at the genome. If they picked BsaI & BmBI with knowledge of the SARS-CoV-2 genome, that doesn't dodge the multiple comparisons problem and the p-values aren't reliable. I guess it depends on how many other commonly used type IIS endonucleases there are. The authors use 214 to generate their null hypothesis distribution for the CoV restriction maps but say only 6 are specifically amenable to BAC cloning.
The "wild type distribution" null distribution for fragment length (Figure 3C) being a simulation (permutation of known CoV genomes, split at randomly selected restriction sites) bothers me. On the first read I thought it was a distribution of fragment lengths in real viruses. Does synthesizing virtual genomes by permutation produce a realistic distribution of fragment lengths?