Palatin –like PhosphoLipaseA2Domain –Containing Protein-8(PNPLA8)alias Ca2+ independent phospholipase A2γ(iPLA2γ)is the one that is restricted to the mitochondrial matrix or peroxisomes where it might demonstrate its individual action of cleaving of the phospholipid side chain from sn1 awa sn2 position, leading to liberation of either saturated FAs or poly unsaturated FAs(PUFA)that include oxidized fatty acids. Furthermore iPLA2γ gets directly activated by H2O2 as well as thus get stimulated by redox signaling or oxidative stress. This redox stimulation allows the anti oxidant synergism with the mitochondrial uncoupling protein(UCPs)or other SLC25 mitochondrial family agents acting as carriers by the FA- modulated protonophoretic action also termed mild uncoupling which results in reduction of mitochondrial superoxide generation. This mode permits for the sustenance of the steady state redox status of the cell. Other than its anti oxidant part here the association of iPLA2γ to lipid peroxidation is reviewed here as iPLA2γ gets alternatively stimulated by cardiolipin hydroperoxides in addition to supposedly by structural changes of the lipid bilayer secondary to lipid peroxidation. Rest of iPLA2γ part are mitochondrial (or peroxisomal) membranes besides the production of particular lipid second messengers. Hence like at the time of FAs β oxidationin case of pancreatic β cells, H2O2 stimulated iPLA2γ provides the G- protein coupled receptor (GPR40)metabotropic receptor for multiplication of FA- stimulated insulin liberation. Moreover the cytoshielding part of iPLA2γ in the heart as well as brain,along with role in brown adipose tissue (BAT) metabolism is further detailed. The major work in this field has been by the groups of Jezek P from Chez and Gross RW, Mancuso DJ gourps. Thus this knowledge gives further insight in unraveling the alterations in lipid metabolism in diseases like obesity, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepapititis (NASH), where ectopic fat deposition and accumulation is behind the pathophysiology of these diseases, besides understanding the severity of generation of APS Syndrome resulting in life threatening conditions.