Anaplastic lymphoma kinase (Alk) is a receptor tyrosine kinase primarily expressed within the brain, recognized for its pivotal role as an oncogenic driver across various cancers, including neuroblastoma. Recent studies have expanded the current understanding of Alk's function, extending beyond its oncogenic properties to encompass developmental and metabolic functions, suggesting its involvement as a modulator of body weight. Notably, Alk's gain-of-function in Drosophila has been linked to a significant reduction in pupal size. This study aimed to elucidate the signaling pathway between the brain and fat body governed by Alk and identify the molecular players involved using Drosophila as a model organism. Transcriptomic analyses were employed to identify genes upregulated in the fat body under conditions of Alk gain-of-function. Using the Gal4/UAS system, specific genes were manipulated in the fat body based on their upregulation in Alk gain-of-function mutants. Immunofluorescence techniques were utilized to visualize morphological changes in the fat body and the distribution of lipid droplet distribution, which were then quantified and compared to the Alk gain-of-function phenotype. The results demonstrate that Alk gain-of-function mutation disrupts fat body physiology, resulting in an abnormal phenotype. Several genes emerged as potential candidates involved in fat body metabolism, with mthl8 notably upregulated. Targeted expression of mthl8 led to a phenotype like the Alk gain-of-function fat body phenotype, highlighting mthl8 as a potential key player in the Alk-mediated signaling pathway between the brain and fat body. This study provides mechanistic insights into the role of Alk in metabolism.