Autophagy is a critical process in healthy human cells that removes excess organelles and substances while generating energy. But in cancer cells, autophagy can either feed growing tumors—literally supplying energy—or suppress them by clearing out cancer-promoting substances. Recently, researchers examined this process in non-small cell lung cancer (NSCLC) and focused on GNIP1, a TRIM family protein. Other TRIM proteins have been associated with autophagy previously, but this is the first autophagy study to examine GNIP1. GNIP1 expression was elevated in tumor cells from NSCLC patients, and clinically, it was associated with poor prognosis and survival time. Induced overexpression of GNIP1 in cultured NSCLC cells increased the cancerous behaviors proliferation and migration. Additional cell culture experiments indicated that GNIP1 did this by enhancing autophagy. Specifically, GNIP1 mediated the breakdown of the VPS34 complex, an autophagy inhibitor. Further, GNIP1 recruited the proteins BECN1 and LC3B, which play roles in the first key step of autophagy, autophagosome formation. Tests in mice also showed that overexpressing GNIP1 increased autophagy and tumor formation. While more research is needed, these results suggest that GNIP1 is a promising therapeutic target to reduce autophagy and treat NSCLC.