Are there known downsides to removing UV mutation hotspots to prevent some skin cancers (Genetic sunblock)?
Short-wave UV light (UVB and UVC) causes transition mutations at dipyrmidine sequences (ref.). In the work presented on KNSTRN quoted by the OP the authors report that 19 from a panel of 100 squamous cell carcinomas (SCC) contained a mutation in KNSTRN (and furthermore three of these contained no other mutation across the six genes that were analysed (Fig. 1b)). Normalising for ORF length this makes it the 3rd most recurrent mutated gene. It would seem therefore that it a fairly important mutagenic target. In a broadened set of SCCs they found a total of 29 KSTRN mutations, and of these 13 were Ser24Phe (TCC&gt;TTC) mutations, which they refer to as a 'hotspot'.
Accepting the arguments in the answer from @Chris it is still interesting to consider how one might remove such a hotspot. The normal amino acid at this position is a serine. Here is the human codon useage for ser, obtained from here:

TCT 14.6%
TCC 22.0%
TCA 15.0%
TCG  6.0%
AGT 11.9%
AGC 19.4%

It would seem therefore that it would be theoretically possible to edit the Ser24 codon from the UV-sensitive TCC to AGC, essentially eliminating this 'hotspot'.
This, of course, doesn't answer the question - are there downsides to this? I already selected a synonymous codon with a similar frequency of useage so that shouldn't be a problem. However here is an example of a synonymous codon substitution which has an effect upon splicing of the LMNA gene resulting in muscular dystrophy, and the paper cites several other examples of this. (I haven't actually checked to see where the Ser24 codon lies in relation the exon-intron boundaries in the KNSTRN gene.) No doubt there are other mechanisms by which my proposed edit could have unwanted effects. It would have to be tested carefully, and so we come back around to a cost-benefit analysis - would it be worth developing this editing idea (even if it were feasible as a therapy) given that there are clearly many paths to SCC not involving this specific mutation.