AKT1 and neoplasm: It is also known to regulate stress responses through the c-Jun N-terminal kinase (JNK) pathway,[26,27] cytoskeleton rearrangements[28] and plays roles in the AKT pathway, autophagy, and epithelial–mesenchymal transition.[29] Small molecules targeting TNIK have been reported to suppress tumor initiation,[5,23,29] which has been a major impetus in developing second generation kinase inhibitors.