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Here, we aim to enlist computations to discover how same pathway and same-gene mutations, and overexpression can preferentially lead to cancer and NDDs phenotypes, with the overarching goal of applying the learned knowledge to identify likely culpable genes/mutations (Figure 1B)

Investigations Thyroid Ultrasound Subacute phase: Enlarged, hypoechoic gland with hypervascular septae (mimicking Graves disease) Chronic phase: Small, atrophic, hypoechoic gland with no vascularity Suspicion of lymphoma: Patchy hypoechogenicity in an enlarged gland Laboratory Tests TSH: Elevated (often the earliest abnormality) Free T4: Low or normal Antibodies: Thyroid peroxidase antibodies, antithyroglobulin antibodies, and antimicrosomal antibodies: Typically elevated ESR: Often raised, especially in active inflammation Serum Iron studies, Vitamin D levels are also checked Fine Needle Aspiration Cytology (FNAC) Cytology will show significant lymphocytic and plasma cell infiltration with destruction of thyroid follicles

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