MTHFR and hyperhomocysteinemia: Although her folate deficiency did not cause responsive hyperhomocysteinemia, and she did not have pathogenic <i>MTHFR</i> mutations that impair the function of methylenetetrahydrofolate reductase in folate cycle, we suggest that isolated folate deficiency may play a role in adolescent cases of ASAS that, once identified, would require prompt identification and early intervention to improve the prognosis of these patients.