Such a pro-oncogenic function of p62 indicates a major role of p62-mediated caspase-2 proteasomal degradation in lung cancer that is confirmed by excess proteasome activity consistent with proteotoxic stress that has been observed in many tumor cell types expressing oncogenic mutant p53 alleles, including NSCLC [42]. The gene discussed is SQSTM1; the disease is non-small cell lung carcinoma.