For example, IL-10R, WASP, and MEK signaling was not downregulated by application of crizotinib; instead, tumor cells developed resistance to the drug through autocrine IL-10 secretion by ALK+ ALCL cells and activation of IL-10R signaling, which replaced the role of ALK in promoting IL-10R expression, suggesting that cytologic changes caused by ALK led to the emergence of ALK-independent mechanisms of tumor cell survival (59, 68). This evidence concerns the gene WAS and neoplasm.