To find out if mutations in the Myo1C gene in human cancers are associated with pathways known to be affected in NM1 KO mouse embryonic fibroblasts, we next performed single sample gene set enrichment analysis followed by linear regression analysis and found that proliferation, apoptosis, and most importantly glycolysis pathways are upregulated in cancers with Myo1C mutations while mTOR pathway is suppressed in these cancers (Fig. 7c, d). The gene discussed is MTOR; the disease is cancer.