Taken together, the combination of rapamycin with crizotinib had three major molecular effects: (1) rapamycin suppressed mTORC1 mediated signaling (indicated by dephosphorylation of S6K and RPS6); (2) rapamycin sensitized the tumor cells to crizotinib, leading to inactivation of ALK signaling (dephosphorylation of ALK, AKT and STAT3); (3) crizotinib blocked AKT feedback activation induced by rapamycin. The gene discussed is RPS6KB1; the disease is neoplasm.