The addition of the CDK8/19i to everolimus in the LT study restored some of the ST drug response of tumor cells, including upregulation of the TNFA pathway and prevented changes in gene expression that developed in the LT treated tumors and could contribute to the adaptive everolimus resistance, such as upregulation of p38 activator MAP2K6 or downregulation of the proapoptotic gene PMAIP1. Here, MAP2K6 is linked to neoplasm.