The loss of LDAH, a gene coding for a lipid hydrolase, has been linked to an increased risk of PCa in vivo and in vitro [36], and altered methylation patterns of clustered protocadherins, including PCDHGC4, have been observed in various solid cancers [37], while CHST11 [38, 39] and CRABP2 [40] have been suggested as potential diagnostic and therapeutic targets due to their involvement in several processes ranging from cancer cell stemness, EMT, cell proliferation, cell cycle and drug resistance in different entities. The gene discussed is LDAH; the disease is cancer.