Of the remaining genes, PHLDA3 is implicated in tumour suppressor function, is a target of p53 and also impedes somatic cell reprogramming57, whilst LAD1 encodes ladinin-1, a collagenous anchoring filament protein that is involved with the maintenance of cohesion at the dermal-epidermal boundary58, and defects in this gene are related to linear IgA disease, an autoimmune blistering disease59. This evidence concerns the gene LAD1 and neoplasm.