PRKN and hyperlipidemia: Third, we did not determine the potential functional roles of the significant SNPs identified in the development of hyperlipidaemia; thus, the correlation of the findings needs to be validated by further in-depth studies with the incorporation of the genetic information of single-nucleotide mutations in the PRKN–PACRG cluster, their haplotypes, and G × G and G × E interactions via in vitro and in vivo functional studies to verify the effects of this variation at the molecular level, including the effects on transcription and translation.