BACKGROUND: Type 1 diabetes mellitus (T1DM) is a chronic disease in children which is usually caused by autoimmunity that damages pancreatic a and b cells which have functions as blood glucose regulators. Some studies stated that Renalase (RNLS) gene deletion will protect these b cells from autoimmune reactions and Endoplasmic Reticulum (ER) stress. RNLS deletion by genome editing Clustered Regular interspersed Short Palindromic Repeats-CRISPR-related (CRISPR/Cas9) is believed to have the potential to be a therapy for T1DM Patients. AIM: This research was conducted to know the potential of RNLS deletion using the CRISPR/Cas9 as an effective therapy and whether it has a permanent effect on T1DM patients. METHODS: The method applied in this research summarized articles by analyzing the titles and abstracts of various predetermined keywords. In this case, the author chose a full-text article published within the past 10 years by prioritizing searches in the last 5 years through PubMed, Google Scholar, Science Direct, Cochrane, American Diabetes Association, and official guidelines from IDAI. RESULTS: RNLS deletion using CRISPR/Cas9 in mice weakened the response of polyclonal -cell-reactive CD8+ T cells and disrupted the immune recognition to cells so that autoimmune killing did occur. In addition, such deletion prevents RNLS ER stress by increasing the threshold, triggering the unfolded protein response so that ER stress is difficult to occur. RNLS mutations in b cells also increase b cell survivability to oxidative stress. CONCLUSION: b cells RNLS deletion by genome editing CRISPR/Cas9 is effective in protecting b cells from autoimmune reactions and RE stress. However, further research is needed to determine the side effects and safety of its use.

BACKGROUND: Duchenne muscular dystrophy is a neuromuscular disease caused by a deficiency of dystrophin, which causes the skeletal and cardiac muscles to degenerate. Targeted deletion of DMD, RIPK3, and MLKL has been shown in several studies to prevent dystrophin deficiency and necroptosis, a critical hypothesis in the etiology of Duchenne muscular dystrophy. AIM: This research aimed to see if using CRISPR/Cas9 to target DMD, RIPK3, and MLKL is an effective therapeutic and if it has a long-term effect on Duchenne muscular dystrophy. METHODS: Abstracts and titles of articles were searched for specific keywords to summarize them using the method used in this study. The researcher will look over the entire article to see if it is valuable and relevant to the topic. RESULTS: CRISPR/Cas9-mediated genome editing in MDX mice can improve the primary genetic lesions that cause muscular dystrophy (DMD) and prevent disease development. Furthermore, Ripk3/Mlk1 double knockout completely blocked necroptosis susceptibility in necroptosis-sensitive cell lines, each to an indistinguishable degree. CONCLUSION: DMD, RIPK3, and MLKL gene editing by CRISPR/Cas9 is effective dystrophin insufficiency, sarcolemma fragility, poor intracellular signaling, myocyte death, inflammatory infiltration, muscle replacement, and necroptosis. However, more research is needed to determine its side effects and safety.