Further validation by ELISA showed that the level of FBLN1 in the CoA group (8.92 ± 2.36 μg/ml) was significantly higher than that in the control group (6.13 ± 1.94 μg/ml), and the level of ALS in CoA children (348.08 ± 216.74 ng/ml) was significantly lower than the level in normal children (619.46 ± 274.08 ng/ml) (Table 3). This evidence concerns the gene FBLN1 and amyotrophic lateral sclerosis.