This process plays a crucial role in thermogenesis, energy expenditure, and glucose homeostasis, making it as a promising target for addressing obesity and diabetes.[31] Previous studies have suggested that mitochondrial dysfunction is linked to a phenotype marked by the suppression of WAT browning.[26, 32] In eWAT of SRSF1‐deficient mice, we observed exon 6 skipping in Ndufs3 pre‐mRNA along with increased apoptosis‐related proteins, indicating potential impairment in WAT functions (Figure S10, Supporting Information). The gene discussed is SRSF1; the disease is Obesity.