In this work, computational biology methods were applied, following the methodology previously described by our group [10,11], to an in silico analysis of hnRNPA1 protein, which has been described as the cause of familial Amyotrophic Lateral Sclerosis type 20, aiming for a thorough analysis of the protein structure and its natural variants, as well as the effects of structural changes in the disease development. This evidence concerns the gene HNRNPA1 and amyotrophic lateral sclerosis type 20.