More recently, glucosylsphingosine accumulation was demonstrated in a CRISPR-Cas9 model of Gba deficiency (gbaΔ31/Δ31, Table 2, and Supplementary Table S1), which could be rescued by overexpression or infusion of human GBA (Lelieveld et al., 2019). The gene discussed is GBA1; the disease is hyperinsulinemic hypoglycemia, familial, 4.