Third, the functional implication of low fucosyation in gastric cancer is not well investigated. The N-glycan structural alteration of some important receptors might modulate the signal transduction pathway. Future extended clinical study and functional exploration are required to validate the finding revealed in this study and uncover some other yet unknown mechanism involved to elucidate the impacts of glycosyations in carcinogenesis. The risk of mortality in VL has recently increased due to it’s association with HIV infection. It is one of the most neglected parasitic diseases in terms of drug development and there are no licensed vaccines available in the market. At present, VL treatment relies on a handful number of drugs such as pentavalent antimonials, amphotericin-B and its formulations, paromomycin and the only orally administered drug miltefosine. However, none of these drugs are ideal for treatment due to their high toxicity, resistance issues, prohibitive prices, long treatment regimen and mode of administration. Over the past few decades significant improvements have been made in the number of treatments available for VL, with both new drugs and new formulations of old drugs that have been either recently approved or are in clinical trials are now available. Recently, combination therapy using immunomodulators with standard antileishmanial compounds have become increasingly popular and several studies have reported benefits of co-administration of antileishmanial drugs with immunostimulants as they shorten the course of treatment, delay or prevent the emergence of resistance and increase the efficacy of current therapeutic regimen. Imiquimod, a novel immune response activating compound approved by USA Food and Drug Administration is currently being used with paromomycin for successful treatment of cutaneous leishmaniasis. Quassin, fucoidan, and curdlan are other examples of immunomodulators that have recently been explored for their potential to kill the Leishmania parasites by boosting host immunity in experimental models of VL. Since, progression of VL infection is generally associated with down regulation of the host immune system, Leishmania has evolved several skills to inactivate macrophage immune functions to survive inside the cells. The outcome of infection depends on the production and/or secretion of immunosuppressive molecules that includes, transforming growth factor -b, interleukin -10 and prostaglandin E2. These molecules distort the normal immune response by suppressing host-protective microbicidal molecules, including cytokines like interferon -c, IL-1, IL-12, and tumor necrosis factor-a, and reactive nitrogen and oxygen species. Growing body of evidences suggest that compounds/agents that boost host cell activation by Th1 biased immune response might be useful as potential therapeutic agents for treatment of experimental VL.