While studies are inconclusive, autologous stem cell bone marrow transplantation appears to prolong survival in early treatment failure patients who are healthy enough to withstand this therapy. Unfit patients may benefit from initial treatment with obinutuzumab plus bendamustine followed by maintenance treatment with obinutuzumab (if they have not been treated previously with obinutuzumab).Other mostly experimental treatments currently under study in patients with multiple treatment failures include: 1) Phosphoinositide 3-kinase inhibitors such as copanlisib, duvelisib, and idelalisib which block the phosphoinositide 3-kinase signaling pathway that promotes the survival, proliferation, and other potentially malignant behaviors of cells; 2) infusion of tisagenlecleucel chimeric antigen receptor T cells (i.e. CAR T cells) (i.e. T cells that have been isolated from patients, engineered to express a receptor for the CD19 protein on, and thereby kill, T cells, and then infused back into the donor patient); 3) Bruons tyrosine kinase inhibitor, ibrutinib, to block the B-cell maturating actions of this kianase; 4) BCL inhibitor  venetoclax to block Bcl2s action in promoting B-cell survival and proliferation; 5) histone deacetylase inhibitors abexinostat and tazemetostat to modify the expression of various genes; and 6) Checkpoint inhibitors nivolumab, pidilizumab, and pembrolizumab to promote the immune systems ability to suppress cancer cell growth. In preliminary studies on FL patients who were known or thought to be refractor to more conventional therapies these drugs, when combined with more conventional drugs, particularly rituximab, produced promising results.
Farber disease (also known as Farbers lipogranulomatosis, acid ceramidase deficiency, "Lipogranulomatosis", and ASAH1-related disorders) is an extremely rare, progressive, autosomal recessive lysosomal storage disease caused by a deficiency of the acid ceramidase enzyme. Acid ceramidase is responsible for breaking down ceramide into sphingosine and fatty acid. When the enzyme is deficient, this leads to an accumulation of fatty material (called ceramide) in the lysosomes of the cells, leading to the signs and symptoms of this disorder. Signs and Symptoms
The symptoms of Farber disease develop over time. The onset of symptoms and how quickly they progress vary from person to person.The most common symptoms include:
Bumps under the skin located at pressure points and joints, also called subcutaneous nodules, lipogranulomas, or granulomas
Swollen, painful joints with progressive limitation of range of motion resulting in contracture
Hoarse voice/cryOther symptoms observed in some individuals with Farber disease include:
Respiratory disease, e.g. lung infections, labored breathing, respiratory distress
Central nervous system disease, e.g. developmental delay, muscle weakness, seizures
Systemic inflammation
Failure to thrive
Bone disease, e.g. erosion of bone near joints, osteoporosis, peripheral osteolysis
Enlarged liver (hepatomegaly)
Eye disease, e.g. cherry-red spot, corneal opacities

Genetics
Farber disease is caused by variants in the ASAH1 gene. This gene codes for the acid ceramidase enzyme. Individuals with Farber disease have two copies of this gene that are not functioning properly leading to the enzyme deficiency. Over 73 different gene variants have been reported to cause Farber disease. No definitive genotype-phenotype correlations are known.Farber disease is inherited in an autosomal recessive manner.