There were increased caspase-1 activation and IL-1β production in the colon of Dox-treated iUVRAGFS as compared to control mice, which correlated with suppressed autophagy, as measured by LC3 conversion and p62 turnover (Fig. 5e, h), supporting the concept that disturbed autophagy by UVRAGFS has a mechanistic role in unresolved inflammasome activation and inflammation-associated tumor susceptibility. The gene discussed is MAP1LC3A; the disease is neoplasm.