Gaucher's disease is not very common. Types II and III, which involve less than 1 in 100,000 people, are extremely uncommon and have various degrees of neurologic system involvement. The most present lysosomal storage disorder is type I Gaucher's disease, which affects mostly adults. Although Type I illness is still rare affecting roughly 1 in 30 to 40000 people, experience in the UK indicated that over 90 to 95% of patients have it. Cellular malfunction and behavioral issues emerge from the lysosomal dysfunction that follows. In sphingolipidoses, Gaucher disease is the most prevalent. In 1882, Philippe Gaucher discovered a patient that had significant splenomegaly who lacked leukemia. GBA1 gene mutations on the chromosome cause GD, a rare, autosomal, recessive inherited condition. The major decrease in GCase activity occurs by mutations in the GBA1 gene. This deficiency's effects are generally ascribed to the deposits of the GCase substrate, GlcCer, in macrophages, which leads them to change into Gaucher cells, as per the most recent studies, Gaucher cells are a new M2 subpopulation that arises from another differentiation mechanism and is not just the consequence of macrophage cell transformation. Other than of getting fully polarized and receiving a specific type of cell such as M1 or M2, macrophages can exhibit a variety of functional stages of polarization. Ferritin binds iron and stops toxicity to cell their supporters. In GD, hepcidin earnings, which prohibits intestinal absorption of iron, is up, while ferritin levels in Gaucher cells are enhanced. Certain cytokines (IL-6 and IL-1β) in Gaucher cells can boost the transcription of the hepcidin gene. Establishing poor G Case activity in total leukocytes, mononuclear cells, or cultured fibroblasts must be done to prove the diagnosis of GD. In many instances, the other enzyme activity is 10% to 15% of the normal value.