The splicing variant D of the TAK1 gene is activated by short double-stranded RNAs in a sequence specific manner. Activation of TAK1-D leads to the downstream activation of the p38 MAPK and of SAPK/JNK but not the NFκB pathway. The current invention therefore provides a method of inducing apoptosis and/or cell cycle arrest in a cancer cell comprising contacting said cell with an agonist of Tak1-D function. The invention further provides a method of modulating inflammation and the treatment of cancer by the administration of an agonist of Tak1-D function or expression. In yet another aspect, the invention provides a method of inducing p38 MAPK and SAPK/JNK signaling in a cell comprising contacting said cell with an agonist of Tak1-D function or expression.
