Activation of the p38γ and δ isoforms abolishes the CSC properties and tumor-initiating ability of non-small cell lung cancer (NSCLC) cells through ubiquitination and degradation of stemness proteins SOX2, OCT4, Nanog, KLF4, and c-MYC through MK2-mediated phosphorylation of Hsp27, a fundamental component of the proteasomal degradation machinery [70]. Here, MYC is linked to non-small cell lung carcinoma.