Using quasi-genetic studies with knockdown of cPLA2 or overexpression of LPCAT1 specifically in SCD BMT chimeras, we demonstrated that correcting the imbalance of Lands’ cycle by reducing cPLA2 activity or inducing LPCAT1 activity significantly attenuated sickling, hemolysis, inflammation and tissue damage by reducing erythrocyte membrane LysoPC, the ratio of LysoPC/PC and LysoPC/PL and circulating AA levels. The gene discussed is LPCAT1; the disease is Schnyder corneal dystrophy.