Interestingly, reducing C9orf72 protein levels was able to alleviate the lysosomal defects caused by TMEM106B overexpression in cells [409], while a reduction of TMEM106B could only partially rescue neuronal loss in a C9orf72 ALS/FTD mouse model [414] adding another layer to the complex relationship between GRN, C9orf72 and TMEM106B in lysosomal health and neurodegeneration. The gene discussed is C9orf72; the disease is frontotemporal dementia.