It was consistent with an increase in a decrease and professional apoptotic protein Bax in anti apoptotic protein HCV NS5A protease inhibitor Bcl 2. p38 and Akt inhibitors block molecular targets involved in cell survival pathway The prototypic pathways that promote cell survival are the phosphoinositide kinase/Akt/ mammalian target of rapamycin pathways, which are constitutively activated in several cancer types including those that develop in the skin. In this research, using western blot analysis and immunostaining we found increased quantities of p Akt in CsA treated group. Earlier, CsA therapy was shown to produce Akt pathway. But, here we found that its inhibitor triciribine reduced p Akt and its downstream target p mTOR. Similar results were obtained following inhibition of p38 by SB 203580. Moreover, the mixed inhibition of both p38 and Akt in CsA treated Infectious causes of cancer animals was more powerful and more somewhat paid down p p38, p Akt and p mTOR in comparison with CsA treatment group. We also found paid down expression of phosphorylated MAPK activated protein kinase 2, a downstream target of p38 in tumors treated with one of these inhibitors alone or in combination. Akt and p38 inhibitors As compared to CsA treatment group, treatment of CsA administered animals with p38 and Akt inhibitors enhanced expression of E cadherin, an epithelial marker and decreased vimentin, a marker restore the epithelial phenotype by lowering EMT. N cadherin, yet another mesenchymal gun was also decreased significantly following treatment with one of these agents alone or in combination. Similar decrease was noted in MMP 2 and MMP 9 expression following these treatments. It is recognized that immune suppressive drugs improve cutaneous and other neoplasms. These drugs by directly reaching cancer cells enhance their invasiveness and metastatic potential. The others and we have shown that the mechanisms underlying these changes include modulation k48 ubiquitin of NFAT signaling pathways that regulate expression of numerous cytokines, cell pattern, apoptosis and differentiation related genes. We also showed that CsA by regulating TGFB dependent signaling pathway encourages EMT and modulate invasive potential of cutaneous SCCs. In this regard, our studies more demonstrated an involvement of TAK1/TAB1 signaling pathway, which by regulating MAPK and Akt augment cancer cell survival. Here, we demonstrated that mixed inhibition of p38 and Akt signaling pathways abrogates CsA mediated cancer progression. The process through which this combination works appears to involve inhibition of growth and enhancement of apoptosis. It is likely that these agents together target cell survival and proliferation related signaling pathways to attenuate the development of these lesions. But, the actual molecular mechanism remains to be examined. In conclusion, our data provide an identification of novel molecular therapeutic targets for cutaneous SCCs in OTRs.