Parkinson’s Disease (PD) is the second most common neurodegenerative disorder that effects approximately 10 million people worldwide. A compelling pathological hallmark of PD is mitochondria dysfunction, which drives neurodegeneration through energy failure, oxidative stress and inflammation. Mitophagy, the selective clearance of damaged mitochondria, is disrupted in PINK1 and Parkin familial mutations of PD. By targeting alternative forms of mitophagy through the mitophagy receptors BNIP3 and NIX, that do not rely on PINK1 and Parkin, we aim to delineate new mechanistic insights into this receptor mediated pathway which will be beneficial for PD treatment. By stimulating the cells hypoxic response, using a prolyl-4-hydroxylase inhibitor, BNIP3 and NIX are transcriptionally upregulated, accumulating on mitochondria and subsequently inducing mitophagy. We used this drug in an unbiased whole-genome CRISPR screen to identify novel regulators of the BNIP3/NIX pathway. Surprisingly, we’ve identified multiple components of the ubiquitin system (including E2, E3 and deubiquitinase) in a pathway that was previously thought to be ubiquitin independent. The E3 ligase MIB2 is an important regulator of this pathway, and we aim to elucidate the exact mechanism of MIB2s involvement in BNIP3/NIX mitophagy.