Similarly, variations in the transcription factors GLIS3, NEUROD1, NEUROG3, NKX2-2, or MNX1 can result in malformed or absent β cells that do not secrete insulin. EIF2AK3 variants can exacerbate ER stress causing β-cell death, skeletal issues, and liver dysfunction. Some variations in immune gene FOXP3 can cause IPEX syndrome, a severe and multifaceted disease that includes neonatal diabetes among its symptoms.Two genes in this region that can be associated with TNDM:
ZAC and HYMAI Genes
ZAC is a zinc-finger protein that controls apoptosis (programmed cell death) and cell cycle arrest (cell division and duplication of DNA stops  when the cell detects cell damage or defects) in PLAG1
(pleomorphic adenoma gene-like 1). PLAG1  is a transcription regulator of the type 1 receptor for pituitary adenylated cyclase-activating polypeptide (is a polypeptide that activates adenylate cyclase and increases the cyclic adenosine monophosphate or cAMP. cAMP is a second messenger that is used for neighboring cells to perform  signal transduction in targeted cells), which is important for insulin secretion regulation. The function of the HYMAI (hydatiform mole-associated and imprinted transcript) is unknown.Second, chromosome 6q24-TNDM is caused by over-expression of imprinted genes at 6q24 (PLAGL1 [ZAC] and HYMAI). It was discovered that a differentially methylated region (DMR) is present within the shared promoter of these genes. Generally the expression of the mothers alleles of PLAGL1 and HYMAI are blocked or not expressed by DMR methylation and only the fathers alleles of PLAG1 and HYMA1 are expressed.
Acute interstitial pneumonitis is a rare, severe lung disease that usually affects otherwise healthy individuals. There is no known cause or cure. Acute interstitial pneumonitis is often categorized as both an interstitial lung disease and a form of acute respiratory distress syndrome (ARDS) but it is distinguished from the chronic forms of interstitial pneumonia such as idiopathic pulmonary fibrosis. Symptoms and signs
The most common symptoms of acute interstitial pneumonitis are highly productive cough with expectoration of thick mucus, fever, and difficulties breathing. These often occur over a period of one to two weeks before medical attention is sought. The presence of fluid means the person experiences a feeling similar to drowning. Difficulties breathing can quickly progress to an inability to breathe without support (respiratory failure).Acute interstitial pneumonitis typically progresses rapidly, with hospitalization and mechanical ventilation often required only days to weeks after initial symptoms of cough, fever, and difficulties breathing develop. Diagnosis
Rapid progression from initial symptoms to respiratory failure is a key feature. An X-ray that shows ARDS is necessary for diagnosis (fluid in the small air sacs (alveoli) in both lungs). In addition, a biopsy of the lung that shows organizing diffuse alveolar damage is required for diagnosis. This type of alveolar damage can be attributed to nonconcentrated and nonlocalized alveoli damage, marked alveolar septal edema with inflammatory cell infiltration, fibroblast proliferation, occasional hyaline membranes, and thickening of the alveolar walls. The septa are lined with atypical, hyperplastic type II pneumocytes, thus leading to the collapse of airspaces.