These results indicate that p38 activation by MKK3E reverses the stimulatory effect of WIP1, and that p38 suppression by MKK6A reverses the inhibitory effect of WIP1 shRNAs on stemness-related protein expression and CSC properties, demonstrating that WIP1 acts upstream of p38 to promote stemness-related protein expression and CSC properties in NSCLC cells. The gene discussed is PPM1D; the disease is non-small cell lung carcinoma.