studies have focused on genes involved in susceptibility to other mycobacterial infections, finding susceptibility to Buruli ulcer may be linked to variants in six immunity-related genes: SLC11A1, PRKN, NOD2, ATG16L1, iNOS, and IFNG, as well as in two long non-coding RNAs. A genome-wide association study linked resistance to Buruli ulcer to a variant of ATG16L1 associated with susceptibility to Crohn's disease. Diagnosis As Buruli ulcer most commonly occurs in low-resource settings, treatment is often initiated by a clinician based on signs and symptoms alone. Where available, diagnosis may then be confirmed by polymerase chain reaction (PCR) to detect M. ulcerans DNA or microscopy to detect mycobacteria. The gold standard test is real-time PCR to detect a DNA sequence termed IS2404 that is unique to M. ulcerans. This method detects M. ulcerans in 54–84% of infected people, and is highly specific to M. ulcerans. In wealthier healthcare settings, diagnosis is routinely based on PCR results. In low-resource settings, PCR is often unavailable, or can only be performed later at a centralized diagnostic laboratory. For microscopy, fluid is typically taken from the ulcer's edge by fine-needle aspiration or by swabbing the edge of the ulcer. The fluid is then stained with the Ziehl–Neelsen stain which makes mycobacteria visible. In practice microscopy detects M. ulcerans in just 30–40% of infected people, making it a relatively insensitive diagnostic test. For many bacterial infections, the gold standard for diagnosis is isolating and growing the infective organism in laboratory media. M. ulcerans can be grown in laboratory media, but its extremely slow growth rate prevents this from being used diagnostically; even under optimal growth conditions, the bacteria must grow for 9 to 12 weeks before they can be easily detected and identified. Another method of diagnosis is to take a tissue sample from the ulcer and examine it under histological stains. This requires more invasive sampling and review by a trained pathologist, and is rarely used in places where Buruli ulcer is endemic. Other ulcerative diseases can appear similar to Buruli ulcer at its various stages. The nodule that appears early in the disease can resemble a bug bite, sebaceous cyst, lipoma, onchocerciasis, other mycobacterial skin infections, or an enlarged lymph node. Skin ulcers can resemble those caused by leishmaniasis, yaws, squamous cell carcinoma, Haemophilus ducreyi infection, and tissue death due to poor circulation. More diffuse lesions can resemble cellulitis and fungal infections of the skin.