Increases in long-chain Cer, specifically 16:0 species, are associated with dysregulated apoptosis.73 In immortalized human cervical cancer cells (HeLa cells), increased expression of CerS2 (C22–C24) has protective effects against apoptosis, whilst an increased expression of CerS5 (C16) promotes apoptosis.74 These cellular studies highlight the possible implications of any modifications to CerS2 in Huntington’s caudate. This evidence concerns the gene CERS2 and cervical cancer.