Their mechanisms span several cancer hallmarks, such as Ca2+-channeled proliferation (e.g., ORAI1 and ORAI3), lysosomal exocytosis-driven metastasis (e.g., TMEM106B), EMT (e.g., TMEM52B, TMEM100, TMEM106A, TMEM229A, TMEM139, TMEM158, TMEM160, and TMEM176B), regulation of programed cell death (e.g., TMEM173, TMEM45B, TMEM48, TMEM100, TMEM106A, TMEM164, TMEM166, TMEM176A, TMEM196, TMEM158, and TMEM215), Wnt and β-catenin modulation (e.g., TMEM33 and TMEM100), metabolic rewiring (e.g., TMEM14A and TMEM160), and immune checkpoint reprogramming (e.g., ORAI1 and TMEM184A). This evidence concerns the gene TMEM229A and cancer.