In conclusion, the SPHK1 mutations studied do not destabilize the protein's overall structure but produce localized changes that may be biologically relevant. These results underscore the importance of combining computational modeling with conservation and functional prediction tools to better understand cancer-associated mutations. They also support the notion that mutations in SPHK1 may not be neutral passengers but rather subtle modulators of tumor biology. 

Additional biochemical and functional studies are needed to confirm these hypotheses and evaluate the therapeutic potential of targeting these variants in prostate cancer.