Having found that the treatment of cathepsin L inhibitor in the HMC3 cells increased both GCase protein level and lysosomal GCase activity, we asked whether the cathepsin L inhibitor can correct reduced GCase protein level and GCase activity in cellular models of GCase deficiency, such as human fibroblast cells derived from a patient with GD carrying a homozygous L444P mutation (GBA1 L444P/L444P) (72). This evidence concerns the gene GBA1 and hyperinsulinemic hypoglycemia, familial, 4.