In the present study on cell migration, we discovered that siRNA CD44 cells were significantly less migratory in comparison to the HT29 vector cells that overexpressed natural product library, indicating that a reduction in CD44 levels could result in altered migration potential in the human colon cancer cells. Such improved migratory potential may be as a result of interactions/alterations in-the levels of Lyn, cofilin and AKT G observed. However, the position of the phosphorylated cofilin and Lyn in colaboration with cell migration and AKT P needs further elucidation. To summarize, we’re ergo suggesting a model where CD44 because relationship with Lyn prevents the local pool of Lyn to adequately activate AKT. This results in increased cell motility and cofilin upregulation. Conversely, lack of CD44 results in the bioavailability of Lyn to trigger AKT leading to cofilin downregulation and reduced cell migration. Inhibition of AKT G by LY294002, which led to both cofilin and Lyn term being stabilized further strengthens the above idea. Today’s experimental study ergo brings us to suggest that CD44 is involved in adjusting the online motility/migration of human colon cancer cells via alterations in quantities of Lyn kinase, triggered AKT and cofilin. Anaplastic large cell lymphoma was described in 1985 by Stein Immune system and his co workers, who claimed that the part of nonHodgkin lymphoma expressed the CD30/Ki 1 antigen with repeated cohesive proliferation and lymph node infiltration. It is now agreed that ALCL is a T/null cell neoplasm often seen as a the aberrant anaplastic lymphoma kinase protein expression, which benefits from chromosome translocation relating to the ALK gene. About 80-20 of genetic alterations include t translocation between the ALK gene on chromosome 2p23 and the nucleophosmin gene on chromosome 5q35. More over, a few studies demonstrate that the remaining 20% of ALK positive ALCLs are related to other translocations in the ALK gene at 2p23, Many of these translocations contain t creating the TPM3 ALK protein, t creating the TPM4 ALK Protein, t creating the TFG ALK protein, t creating the CLTC ALK protein, inv2 creating the ATIC ALK protein, and t creating the ALO17 ALK protein. All translocations include ALK boasts significant oncogenic potential ensuing fromthe constitutive activation of the tyrosine kinase order BI-1356 ALK. That kinase activation may induce cellular change, safety from apoptosis, growth factor independent growth, and resistance to therapeutic drugs. In line with the current World Health Organization classification of lymphomas, ALCL may be sub-divided into two biologic subtypes in line with the presence or absence of aberrant expression of ALK. More over, studies have shown that ALK good ALCL indicates different pathological, molecular and clinical characteristics, and suggest that it is a distinct entity.