Although the biology and molecular biology underlying the utility of APC at the PAR1 target for ALS is strong, the uncontrolled bleeding complication of wild-type APC is unacceptable, and so the development of anticoagulation-deficient variants such as 3K3A-APC have apparently eliminated this issue; however, 3K3A-APC is a protein with a molecular mass of 62 kDa, essentially the same as wild-type PC. This evidence concerns the gene MARK2 and amyotrophic lateral sclerosis.