Lack of a visible phenotype in mtm mutants and the level of endogenous PtdIns5P not significantly lower than in fresh wild type cells suggest that the AtMTM1 function is not essential for the cellular homeostasis in non-stressed cells, in stark contrast with humans where myotubularin deficiency is implicated in severe muscle dystrophy, neuronal diseases, and leukemia [1], [3], [31]. Here, MTM1 is linked to leukemia.