SLCO2A1 and primary hypertrophic osteoarthropathy: As for individuals with heterozygous SLCO2A1 mutations, they either showed distal clubbing or no clinical abnormality, clearly suggesting a certain level of PGE2 uptake and metabolism that define the phenotypic consequence, or there might be the involvement of some factors regulating either PGE2 synthesis, degradation, or signaling that might influence the pathogenesis of PHO and distal clubbing [7].