Since mCRPC relies on de novo synthesis of cholesterol [48], PS showed promise to reduce this PC aggressive phenotype recurrences as a small molecule that can act intracellularly on the PCSK9-LDLR axis and extracellularly, unlike the FDA-approved mAbs, which act only at the extracellular level because they lack the ability to enter PC cells due to their large molecular size [20,23,36]. This evidence concerns the gene PCSK9 and pachyonychia congenita.