In turn, this has been associated with mitochondrial dysfunction and the release of ATP, NAD+, and the caspase-independent nucleases AIF and endonuclease G. RARγ antagonist treated PCa cells growth arrested in G1 of cell cycle and cell death was mitochondria depolarisation-dependent and cellular DNA fragmentation occurred that was caspase-independent (Keedwell et al., 2004; Petrie et al., 2020). The gene discussed is RARG; the disease is posterior cortical atrophy.