However, some authors pointed to cysteine cathepsins B and L (CatB/L; Figure 4) as the main lysosomal enzyme(s) involved in the abnormalities of intracellular cholesterol trafficking related to AD-like features, since unlike CatD, the CatB/L inhibition in SH-SY5Y human neuroblastoma cells by PADK-treatment or its genetic ablation in CatB(−/−)/L(−/−) MEFs resembled NPC disease features (e.g., lysosomal dysfunction by accumulation of both cholesterol and NPC1; and downregulation of ABCA1 expression) and promotes amyloidogenesis assessed by BACE1 and APP-CTFs accumulation (Cermak et al., 2016). This evidence concerns the gene ABCA1 and Alzheimer disease.