ALK and neoplasm: Low-dose 5-aza-Cdr treatment of ALCL cell lines and xenograft mouse models also induced the demethylation and re-expression of p16INK4A [132] and the restoration of shp1, which is known to have a tumour suppressor function associated with the downregulation of JAK3/STAT3 signalling in ALK-positive anaplastic large-cell lymphoma [133].