miR-101 was found to be down-regulated in ALK(+) and (−) human ALCL and CD4/NPM/ALK transgenic mouse models, but its forced expression increased the number of cells arrested in G1 phase of the cell cycle only in ALK(+) and not in ALK(−) ALCL cell lines The serine/threonine kinase mTOR was shown to be targeted by miR-101, and its inhibition led to reduced tumor growth in engrafted ALCL mouse models, suggesting that mTOR inhibitors may offer a viable therapeutic strategy [31]. This evidence concerns the gene MARK2 and anaplastic large cell lymphoma.