The variants of BMPR2 in childhood-onset PAH include missense mutations resulting in the substitutions of amino acids and nonsense mutations, the insertions or deletions of small nucleotides leading to frameshift mutations, gene rearrangements, and splice-site mutations leading to premature protein truncation (Machado et al., 2015; Southgate et al., 2020). This evidence concerns the gene BMPR2 and pulmonary arterial hypertension.