With regards to CRABP1 modulating CaMKII signaling, we have reported two spontaneously developed human disease-mimicking phenotypes of CKO mice; both are associated with aberrant CaMKII activation and cytotoxicity, i.e., cardiomyopathy/heart failure caused by cardiomyocyte apoptosis and death [7] and ALS-like motor deterioration caused by MN death/loss [10]. Here, CAMK2G is linked to amyotrophic lateral sclerosis.